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Displaying publications 41 - 60 of 122 in total

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Antiphospholipid antibodies and antiphospholipid syndrome in cancer: Uninvited guests in troubled times

Islam MA

Semin Cancer Biol, 2020 08;64:108-113.
PMID: 31351197 DOI: 10.1016/j.semcancer.2019.07.019

Antiphospholipid antibodies (aPLs) are autoantibodies with laboratory significance in developing thrombosis and pregnancy morbidity in antiphospholipid syndrome (APS). High prevalence of aPLs namely - anticardiolipin, anti-β2-glycoprotein I, lupus anticoagulant, antiphosphatidylcholine, antiphosphatidylserine, antiphosphatidylinositol, antiphosphatidylethanolamine and antiprothrombin antibodies have been observed in patients with different types of haematological malignancies and solid tumours. Although cancer patients have high risk of developing thrombosis, the risk becomes even higher in aPLs carriers. Although the relationship between aPLs and cancer has to be further investigated, however, the presence of aPLs in neoplastic patients can possibly increase the risk of developing thrombosis. As the pathogenic role of aPLs in cancer is still a matter of debate, more researches should be conducted on the association between the aPLs and malignancies towards the potential impact on understanding the pathogenicity and treatment when cancer and APS coexists.

Matched MeSH terms: Autoantibodies/immunology*
Autoantibodies to tetraspanins (CD9, CD81 and CD82) in demyelinating diseases

Miyaji K, Paul F, Shahrizaila N, Umapathi T, Yuki N

J Neuroimmunol, 2016 Feb 15;291:78-81.
PMID: 26857499 DOI: 10.1016/j.jneuroim.2015.12.012

Tetraspanin family proteins, CD9, CD81 and CD82 are expressed in the oligodendrocytes and Schwann cells. We investigated autoantibodies to tetraspanin proteins in patients with demyelinating diseases. Sera were collected from 119 multiple sclerosis patients, 19 neuromyelitis optica, 42 acute inflammatory demyelinating polyneuropathy, 23 chronic inflammatory demyelinating polyneuropathy and 13 acute motor axonal neuropathy as well as 55 healthy controls. Few multiple sclerosis and acute inflammatory demyelinating polyneuropathy patients had autoantibodies that were weakly reactive to CD9 or CD81 but the significance is unclear. It is unlikely that these autoantibodies are pathogenic or serve as potential biomarkers in demyelinating diseases.

Matched MeSH terms: Autoantibodies/blood*
Fulltext Differences in the Spectrum of Anti-Citrullinated Protein Antibody Fine Specificities Between Malaysian and Swedish Patients With Rheumatoid Arthritis: Implications for Disease Pathogenesis

Too CL, Murad S, Hansson M, Alm LM, Dhaliwal JS, Holmdahl R, et al.

Arthritis Rheumatol, 2017 01;69(1):58-69.
PMID: 27483449 DOI: 10.1002/art.39827

OBJECTIVE: Antibodies to the citrullinated protein antigens (ACPAs) are important in the diagnosis and pathogenesis of rheumatoid arthritis (RA). However, the prevalence of ACPAs with different fine specificities in different populations is unclear. This study sought to examine the fine specificity of the antibody responses toward citrullinated proteins in RA patients from Malaysia, an area where genetic and environmental determinants of RA are different from those in more frequently studied cohorts of Caucasian subjects.
METHODS: A multiplex analytic microarray system was used to analyze the occurrence of antibodies to 10 different citrullinated peptides (filaggrin [fil307-324], vimentin [Vim2-17, Vim60-75], fibrinogen [Fibα563-583, Fibα580-600, Fibβ36-52, Fibβ62-81a, Fibβ62-81b], enolase [Eno5-21], and type II collagen [CitCII355-378]) in serum samples from 4,089 RA patients (1,231 Malaysian and 2,858 Swedish) and 827 healthy control subjects (249 Malaysian and 578 Swedish). The positive reaction threshold for each peptide was set separately for each population based on a specificity of 98%.
RESULTS: Distinct differences in the frequencies of 5 ACPA fine specificities (Vim60-75, Vim2-17, Fibβ62-81b, Eno5-21, and CitCII355-378) were found between the Malaysian and Swedish RA populations, despite a nearly identical percentage of patients in each population who were positive for anti-cyclic citrullinated peptide 2 antibodies. In Malaysian RA patients compared with Swedish RA patients, the frequencies of antibodies to Vim60-75 (54% versus 44%, corrected P [Pcorr ] = 1.06 × 10-8 ) and CitCII355-378 (17% versus 13%, Pcorr = 0.02) were significantly higher, while the frequencies of antibodies to Vim2-17 (25% versus 32%, Pcorr = 1.91 × 10-4 ), Fibβ62-81b (15% versus 30%, Pcorr = 2.47 × 10-22 ), and Eno5-21 (23% versus 50%, Pcorr = 3.64 × 10-57 ) were significantly lower.
CONCLUSION: Serum ACPA fine specificities differ between RA patients in different populations, although the total proportions of individuals positive for ACPAs are similar. Differing patterns of ACPA fine specificity could be attributed to variations in genetic and/or environmental factors.

Matched MeSH terms: Autoantibodies/immunology*
Fulltext Antibodies against testicular germinal cells in lepromatous leprosy

Wall JR, Wright DJ

Clin Exp Immunol, 1974 May;17(1):51-9.
PMID: 4619358

Testicular germinal cell antibodies were found in forty-four out of the fifty-nine patients with lepromatous leprosy and in four out of ten patients with tuberculoid disease. A similar pattern was found in twelve out of 262 control patients and
normal subjects. The antibody was found to be of the IgG class and forty out of forty-nine of these antibodies were shown to be complement fixing. Spermatozoal antibodies were detected in twelve patients, but no ovarian antibodies were found in any specimen. There was no close correlation between erythema nodosum leprosum (ENL) and testicular antibodies. It was found that the characteristic of the testicular antibody in leprosy was its ability to be absorbed by Mycobacterium BCG suspension suggesting that this is another antibody induced by infection. A similar fluorescent pattern was seen in some patients who did not have leprosy, but in these cases it could not be abolished with BCG. It is concluded that autoimmunity may be one of the factors involved in the pathogenesis of orchitis in leprosy.
Study site: MRC Leprosy Research Unit, Sungei Buloh, Selangor, Malaysia.

Matched MeSH terms: Autoantibodies*
Outcome of children with acetylcholine receptor (AChR) antibody positive juvenile myasthenia gravis following thymectomy

Heng HS, Lim M, Absoud M, Austin C, Clarke D, Wraige E, et al.

Neuromuscul Disord, 2014 Jan;24(1):25-30.
PMID: 24239058 DOI: 10.1016/j.nmd.2013.09.013

Most evidence supporting the benefit of thymectomy in juvenile myasthenia gravis (JMG) is extrapolated from adult studies, with only little data concerning paediatric populations. Here we evaluate the outcome of children with generalized JMG who underwent thymectomy between 1996 and 2010 at 2 tertiary paediatric neurology referral centres in the United Kingdom. Twenty patients (15 female, 5 male), aged 13months to 15.5years (median 10.4years) at disease onset, were identified. Prior to thymectomy, disease severity was graded as IIb in 3, III in 11, and IV in 6 patients according to the Osserman classification. All demonstrated positive anti-acetylcholine receptor (AChR) antibody titres. All patients received pyridostigmine and 14 received additional steroid therapy. Transternal thymectomy was performed at the age of 2.7-16.6years (median 11.1years). At the last follow-up (10months to 10.9years, median 2.7years, after thymectomy), the majority of children demonstrated substantial improvement, although some had required additional immune-modulatory therapies. About one third achieved complete remission. The postoperative morbidity was low. No benefit was observed in one patient with thymoma. We conclude that thymectomy should be considered as a treatment option early in the course of generalised AChR antibody-positive JMG.

Matched MeSH terms: Autoantibodies/blood
Is hyaluronic acid filler still a potential risk factor for an autoimmune reaction?

Aljawhar NM, Sharquie IK

Med J Malaysia, 2020 07;75(4):363-367.
PMID: 32723995

BACKGROUND: Rejuvenation of the skin with hyaluronic acid (HA) filler is considered to be one of the most favourable procedures in the field of aesthetics. Nevertheless, some adverse effects still occur though infrequently, and are associated with its use. Previous research has suggested that HA filler may stimulate antibodies. Consequently, an investigation of the immune interactions associated with use of HA filler is an important area for investigation.
OBJECTIVES: The aim of this research is to investigate whether HA filler influences the initiation of an autoimmune reaction in healthy women who had received HA filler by screening for autoantibodies in the blood. Results will be compared with agematched apparently healthy control women who did not receive the filler.
METHODS: Serum samples were obtained from 44 females who had received HA filler and 44 females who had not as a control group. The enzyme-linked immunosorbent assay (ELISA) technique was utilised to measure serum concentrations of anti- Thyroglobulin (Tg), anti -thyroid peroxidase (TPO), rheumatoid factor (RF), anti-nuclear antibody (ANA) and anticentromeres.
RESULTS: The number of women who tested positive for the measured autoantibodies was not statistically significant (p=0.803) between those who had received HA filler (n=10/44, 25%) and the control group (n=11/44, 22.7%).
CONCLUSION: Based on our result HA filler procedures do not induce an autoimmune reaction in women who received HA filler compared to controls. And consequently, HA filler procedures are relatively safe, and these results contradict the findings of other non-controlled works.

Matched MeSH terms: Autoantibodies/blood
IDIOPATHIC AUTO-IMMUNE HAEMOLYTIC ANAEMIA IN MALAYA

LIE-INJOLUAN EN, PILLAY RP

Acta Haematol., 1964 May;31:282-8.
PMID: 14172696
Matched MeSH terms: Autoantibodies*
Autoimmune antithyroid antibodies with special reference to their presence in human patients in Singapore

STEIN J, STEIN B, YU M, CHEE M, CHEW BK

Med J Malaysia, 1963 Dec;18:116-21.
PMID: 14117279
Matched MeSH terms: Autoantibodies*
Characterisation of maternal human leukocyte antigen class I antibodies in suspected foetal and neonatal alloimmune thrombocytopenia

Refsum E, Mörtberg A, Dahl J, Meinke S, Auvinen MK, Westgren M, et al.

Transfus Med, 2017 Feb;27(1):43-51.
PMID: 27862486 DOI: 10.1111/tme.12375

OBJECTIVES: To investigate the specificities and level of HLA class I antibodies in selected cases referred for suspected foetal and neonatal alloimmune thrombocytopenia (FNAIT).
BACKGROUND: FNAIT occurs in 1 : 1-2000 live births, whereas maternal immunisation against human leukocyte antigen (HLA) class I is common. Whether HLA class I antibodies alone can cause FNAIT is debatable.
MATERIAL AND METHODS: A total of 260 patient samples were referred between 2007 and 2012. Referrals with maternal HLA class I antibodies and no other cause for the neonatal thrombocytopenia were included for analysis (cases, n = 23). HPA-1a negative mothers were excluded. Control groups were screened positive mothers of healthy neonates (controls, n = 33) and female blood donors (blood donors, n = 19). LABScreen single antigen HLA class I beads was used for antibody analysis. Clinical records were reviewed for cases.
RESULTS: All groups had broad antibody reactivity. Cases had more antibodies with high SFI levels compared with the controls (SFI>9999; medians 26, 6 and 0; P

Matched MeSH terms: Autoantibodies/blood*
Eleven episodes of recurrent optic neuritis of the same eye for 22 years eventually diagnosed as neuromyelitis optica spectrum disorder

Yew YC, Hor JY, Lim TT, Kanesalingam R, Ching YM, Arip M, et al.

Mult Scler Relat Disord, 2016 Nov;10:22-25.
PMID: 27919493 DOI: 10.1016/j.msard.2016.08.009

It is difficult to predict whether a particular attack of neuromyelitis optica spectrum disorder (NMOSD) will affect the optic nerve [optic neuritis (ON): unilateral or bilateral], spinal cord (myelitis), brain or brainstem, or a combination of the above. We report an interesting case of recurrent ON of the same eye for a total of 11 episodes in a Chinese woman. Over a period of 22 years, the attacks only involved the left eye, and never the right eye and also no myelitis. For a prolonged duration, she was diagnosed as recurrent idiopathic ON. Only until she was tested positive for aquaporin 4 antibody that her diagnosis was revised to NMOSD. Optical coherence tomography revealed thinning of the retinal nerve fibre layer (RNFL) for the affected left eye, while the RNFL thickness was within normal range for the unaffected right eye. The disability accrual in NMOSD is generally considered to be attack-related - without a clinical attack of ON, there shall be no visual impairment, and no significant subclinical thinning of RNFL. Our case is in agreement with this notion. This is in contrast to multiple sclerosis where subclinical RNFL thinning does occur. This case highlights the importance of revisiting and questioning a diagnosis of recurrent idiopathic ON particularly when new diagnostic tools are available.

Matched MeSH terms: Autoantibodies/blood
Fulltext Red cell autoantibodies among thalassaemia patients in Hospital Universiti Sains Malaysia

Noor Haslina MN, Ariffin N, Illuni Hayati I, Rosline H

Singapore Med J, 2007 Oct;48(10):922-5.
PMID: 17909677

Thalassaemia is one of the major public health problems in Malaysia. Regular monthly blood transfusion remains the main treatment for severe thalassaemia patients. One of the complications of blood transfusion is the formation by the recipients of alloantibodies and autoantibodies against red blood cell (RBC) antigen. The purpose of this study was to determine the prevalence of RBC autoantibodies among multiple-transfused thalassaemic patients in our institution and factors that contribute to its development.

Matched MeSH terms: Autoantibodies/blood*
Fulltext The Pathogenesis of the Demyelinating Form of Guillain-Barre Syndrome (GBS): Proteo-peptidomic and Immunological Profiling of Physiological Fluids

Ziganshin RH, Ivanova OM, Lomakin YA, Belogurov AA, Kovalchuk SI, Azarkin IV, et al.

Mol Cell Proteomics, 2016 Jul;15(7):2366-78.
PMID: 27143409 DOI: 10.1074/mcp.M115.056036

Acute inflammatory demyelinating polyneuropathy (AIDP) - the main form of Guillain-Barre syndrome-is a rare and severe disorder of the peripheral nervous system with an unknown etiology. One of the hallmarks of the AIDP pathogenesis is a significantly elevated cerebrospinal fluid (CSF) protein level. In this paper CSF peptidome and proteome in AIDP were analyzed and compared with multiple sclerosis and control patients. A total protein concentration increase was shown to be because of even changes in all proteins rather than some specific response, supporting the hypothesis of protein leakage from blood through the blood-nerve barrier. The elevated CSF protein level in AIDP was complemented by activization of protein degradation and much higher peptidome diversity. Because of the studies of the acute motor axonal form, Guillain-Barre syndrome as a whole is thought to be associated with autoimmune response against neurospecific molecules. Thus, in AIDP, autoantibodies against cell adhesion proteins localized at Ranvier's nodes were suggested as possible targets in AIDP. Indeed, AIDP CSF peptidome analysis revealed cell adhesion proteins degradation, however no reliable dependence on the corresponding autoantibodies levels was found. Proteome analysis revealed overrepresentation of Gene Ontology groups related to responses to bacteria and virus infections, which were earlier suggested as possible AIDP triggers. Immunoglobulin blood serum analysis against most common neuronal viruses did not reveal any specific pathogen; however, AIDP patients were more immunopositive in average and often had polyinfections. Cytokine analysis of both AIDP CSF and blood did not show a systemic adaptive immune response or general inflammation, whereas innate immunity cytokines were up-regulated. To supplement the widely-accepted though still unproven autoimmunity-based AIDP mechanism we propose a hypothesis of the primary peripheral nervous system damaging initiated as an innate immunity-associated local inflammation following neurotropic viruses egress, whereas the autoantibody production might be an optional complementary secondary process.

Matched MeSH terms: Autoantibodies/cerebrospinal fluid*
Fulltext Anti-carbamylated protein antibodies in rheumatoid arthritis patients and their association with rheumatoid factor

Othman MA, Ghazali WSW, Hamid WZWA, Wong KK, Yahya NK

Saudi Med J, 2017 Sep;38(9):934-941.
PMID: 28889152 DOI: 10.15537/smj.2017.9.20841

OBJECTIVES: To evaluate levels of anti-carbamylated protein (anti-CarP) antibodies in rheumatoid arthritis (RA) patients and to determine their association with serological parameters and disease activity. Methods: A cross-sectional study involving 105 multiethnic RA patients (48 rheumatoid factor [RF]-positive and 57 RF-negative patients) was conducted at Hospital Universiti Sains Malaysia, Kelantan, Malaysia, from January 2015 to February 2016. Fifty healthy controls (HCs) were included. C-reactive protein (CRP), RF, anti-cyclic citrullinated peptide (anti-CCP) and anti-CarP antibodies were measured. A health assessment questionnaire (HAQ) was administered to the study participants and 28-joint Disease Activity Score (DAS28) were obtained. Results: The level of anti-CarP antibodies was significantly increased in the RA patients compared with HCs (p=0.042). The presence of anti-CarP antibodies was significantly associated with RF (p=0.019) and the HAQ (p=0.010). A significant association between the presence of anti-CarP antibodies and the DAS28 was not found (p=0.632). Conclusion: Our study provides further evidence that the level of anti-CarP antibodies is significantly elevated in RA patients.

Study site: Rheumatology clinic, Hospital Universiti Sains Malaysia

Matched MeSH terms: Autoantibodies/immunology*
Fulltext Augmentation of Autoantibodies by Helicobacter pylori in Parkinson's Disease Patients May Be Linked to Greater Severity

Suwarnalata G, Tan AH, Isa H, Gudimella R, Anwar A, Loke MF, et al.

PLoS One, 2016;11(4):e0153725.
PMID: 27100827 DOI: 10.1371/journal.pone.0153725

Parkinson's disease (PD) is the second most common chronic and progressive neurodegenerative disorder. Its etiology remains elusive and at present only symptomatic treatments exists. Helicobacter pylori chronically colonizes the gastric mucosa of more than half of the global human population. Interestingly, H. pylori positivity has been found to be associated with greater of PD motor severity. In order to investigate the underlying cause of this association, the Sengenics Immunome protein array, which enables simultaneous screening for autoantibodies against 1636 human proteins, was used to screen the serum of 30 H. pylori-seropositive PD patients (case) and 30 age- and gender-matched H. pylori-seronegative PD patients (control) in this study. In total, 13 significant autoantibodies were identified and ranked, with 8 up-regulated and 5 down-regulated in the case group. Among autoantibodies found to be elevated in H. pylori-seropositive PD were included antibodies that recognize Nuclear factor I subtype A (NFIA), Platelet-derived growth factor B (PDGFB) and Eukaryotic translation initiation factor 4A3 (eIFA3). The presence of elevated autoantibodies against proteins essential for normal neurological functions suggest that immunomodulatory properties of H. pylori may explain the association between H. pylori positivity and greater PD motor severity.

Matched MeSH terms: Autoantibodies/blood; Autoantibodies/immunology*
Fulltext ANA negative (Ro) lupus erythematosus with multiple major organ involvement: a case report

Che Maraina CH, Kamaliah MD, Ishak M

Asian Pac J Allergy Immunol, 2002 Dec;20(4):279-82.
PMID: 12744629

Anti-nuclear antibody (ANA) negative systemic lupus erythematosus (SLE) occurs in about 4-13% of SLE cases. A small group of ANA negative SLE patients with positive anti-Ro antibodies usually present with typical vasculitic skin lesions which can be associated with photosensitivity, renal disease, congenital heart block or neonatal lupus. We present a case of a persistently ANA negative patient who presented with joint pain, rashes, mouth ulcer and alopecia. Clinical diagnosis of systemic lupus erythematosus was made even though ANA was negative. She was started on steroids and went into remission. Later, she developed several episodes of convulsions associated with fever and prominent vasculitic lesions. The patient was also found to have microscopic hematuria, proteinuria, anemia and thrombocytopenia. Renal biopsy showed lupus nephritis class 1B. Due to the prominent skin lesions, we performed anti-extractable nuclear antigens (ENA) antibodies test and anti-Ro turned out to be positive. The final diagnosis was ANA negative SLE (Ro lupus) with cutaneous, renal, musculoskeletal, hematological and cerebral Involvement.

Matched MeSH terms: Autoantibodies/blood; Autoantibodies/immunology
Prevalence and clinical significance of antibodies to ribonucleoproteins in systemic lupus erythematosus in Malaysia

Wang CL, Ooi L, Wang F

Br J Rheumatol, 1996 Feb;35(2):129-32.
PMID: 8612023

One hundred and seventy patients with systemic lupus erythematosus (SLE) were studied for the prevalence of antibodies to the small RNA-associated proteins Ro/SSA, La/SSB, Sm, U1RNP and Sm. The relationship of these autoantibodies to different races, sexes and clinical manifestations of SLE was evaluated. Passive immunodiffusion was employed using human spleen extract as antigen source for Ro and rabbit thymus extract for La, Sm and U1RNP. We found the prevalence of antibodies to be as follows: anti-Ro/SSA, 36%; anti-La/SSB, 8%; anti-Sm, 15% ; anti-U1RNP, 21%. Except for a low prevalence of anti-La, the prevalence of these antibodies was similar to that in Western studies, The prevalence of anti-Ro/SSA is similar to that reported in the Western studies, but lower than that reported in the Oriental patients from Singapore and Hong Kong. Linkages of anti-Ro with anti-La antibodies were usual; however, although anti-Sm antibodies were usually associated with anti-U1RNP, they were more frequently associated with anti-Ro antibodies. The Malay patients had a high prevalence of anti U1RNP compared to other races. No gender difference was detected. Anti-Sm antibody was associated with serositis and anti-U1RNP antibodies with Raynaud's phenomenon. No association was found between the presence of skin renal or cerebral manifestations and any specific antibodies or combination of antibodies.

Matched MeSH terms: Autoantibodies/analysis*; Autoantibodies/immunology
Proactive treatment of angiotensin receptor antibodies in kidney transplantation with plasma exchange and/or candesartan is safe and associated with excellent graft survival at 4 years: A single centre Australian experience

Carroll RP, Deayton S, Emery T, Munasinghe W, Tsiopelas E, Fleet A, et al.

Hum Immunol, 2019 Aug;80(8):573-578.
PMID: 31014826 DOI: 10.1016/j.humimm.2019.04.005

High levels of angiotensin receptor antibodies (ATRab) are associated with acute cellular and humoral rejection, vascular occlusion, de novo human leucocyte antigen donor specific antibody (HLA DSA) and poor graft survival in kidney transplant recipients (KTR). Since 2015 we proactively managed patients "at risk" (AR) with ATRab >17 U/ml with perioperative plasma exchange (PLEX) and/or angiotensin receptor blockade (ARB). 44 patients were treated with this protocol. 265 KTR with ATRab ≤17 U/ml deemed "low risk" (LR) were transplanted under standard conditions. PLEX and ARB were not associated with increased risk of: delayed graft function requiring haemodialysis (HDx), hyperkalaemia >5.5 mmol/l requiring HDx, and the combined clinical end-point of severe hypotension, blood transfusion and re-operation for bleeding. Rejection rates were similar at 90 days: 8/44 (18%) in the AR group and 36/265 (14%) in the LR group (p = 0.350). Death censored graft survival was the same between the AR and LR groups with a 94% 48-month graft survival - hazard ratio (log-rank) 1.16 [95% CI 0.2-5.8] p = 0.844. Proactive treatment of ATRab >17 U/ml with PLEX and/or ARB is not associated with increased rates of perioperative complications and comparable rates of rejection and death censored graft survival at 4 years compared to KTR <17 U/ml ATRab.

Matched MeSH terms: Autoantibodies/metabolism; Autoantibodies/therapeutic use*
Prevalence of AT1R antibody (AT1R-Ab) among Malaysian multi-ethnic population

Jalalonmuhali M, Caroll R, Deayton S, Emery T, Humphreys I, Lim SJ, et al.

Hum Immunol, 2020 Dec;81(12):679-684.
PMID: 32736900 DOI: 10.1016/j.humimm.2020.07.005

BACKGROUND: Angiotensin II type 1 receptor antibody (AT1R-Ab) is a non-HLA antibody that has been reported to cause antibody-mediated rejection and graft loss in kidney transplantation. The prevalence of positive AT1R-Ab varies between 8% and 18% in different regions. Thus, this study aims to determine the prevalence of AT1R-Ab among the Malaysian population.
METHODOLOGY: All sera for AT1R-Ab were collected at the University Malaya Medical Centre (UMMC), Kuala Lumpur, Malaysia. The sera were centrifuged and kept refrigerated at -80 °C before being transported to the South Australian Transplantation and Immunogenetics Laboratory (SATIS). Enzyme-linked immunosorbent assay kit (One Lambda) was used for the detection of AT1R-Ab, and it was performed according to the manufacturer's instructions. The level of >17.1 U/mL was considered to be AT1R-Ab positive; 10.0-17.1 U/mL at risk, and <10.0 U/mL negative.
RESULTS: A total of 115 samples were collected from 99 patients pre and post-kidney transplant recipients. From the pre-transplant sera (n = 68) 17.7% were positive, 35.3% were at risk and 47.0% were negative. The positive AT1R-Ab cohort were relatively younger, with a mean age of 34.7 ± 8.3 years old and statistically significant, with a p-value of 0.028. Among the sera that were tested positive, 19.0% were from the Chinese ethnicity, 6.7% from Malay and 16.7% from Indian. There was no difference in the rejection episodes, persistent or de novo HLA-DSA, and graft function between the group (AT1R-Ab negative vs AT1R-Ab at risk and positive) and the results were consistent in a model adjusted for all potential confounders.
CONCLUSION: The prevalence of positive (>17.1 U/mL) pre-transplant AT1R-Ab was 17.7% and 35.3% were at risk (10.0-17.1 U/mL) in our pre-transplant cohort.

Matched MeSH terms: Autoantibodies/blood*; Autoantibodies/immunology*
Fulltext Association of anti-CLIC2 and anti-HMGB1 autoantibodies with higher disease activity in systemic lupus erythematosus patients

Syahidatulamali CS, Wan Syamimee WG, Azwany YN, Wong KK, Che Maraina CH

J Postgrad Med, 2017 9 2;63(4):257-261.
PMID: 28862243 DOI: 10.4103/jpgm.JPGM_499_16

BACKGROUND: Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by numerous autoantibodies. In this study, we investigated the presence of anti-chloride intracellular channel 2 (anti-CLIC2) and anti-high mobility group box 1 (anti-HMGB1) autoantibodies in SLE patients (n = 43) versus healthy controls ([HCs] n = 43), and their association with serological parameters (antinuclear antibody [ANA], anti-double-stranded DNA [anti-dsDNA], and C-reactive protein [CRP]) and disease activity using Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) score (active or inactive).
SETTINGS AND DESIGN: Case-control study at Rheumatology Clinic of Universiti Sains Malaysia Hospital.
SUBJECTS AND METHODS: The sera of SLE patients and HCs were tested for the presence of anti-CLIC2 and anti-HMGB1 autoantibodies using human recombinant proteins and ELISA methodologies. Other serological parameters were evaluated according to routine procedures, and patients' demographic and clinical data were obtained.
STATISTICAL ANALYSIS: Mann-Whitney U-test, Chi-square test, Fisher's exact test, and receiver operating characteristic analysis.
RESULTS: Anti-CLIC2 autoantibody levels were significantly higher in SLE patients compared to HCs (P = 0.0035), whereas anti-HMGB1 autoantibody levels were not significantly elevated (P = 0.7702). Anti-CLIC2 and anti-HMGB1 autoantibody levels were not associated with ANA pattern, anti-dsDNA, and CRP. Interestingly, SLEDAI score (≥6) was associated with anti-CLIC2 (P = 0.0046) and with anti-HMGB1 (P = 0.0091) autoantibody levels.
CONCLUSION: Our findings support the potential of using anti-CLIC2 autoantibodies as a novel biomarker for SLE patients. Both anti-CLIC2 and anti-HMGB1 autoantibody levels demonstrated potential in monitoring SLE disease activity.

Matched MeSH terms: Autoantibodies/analysis; Autoantibodies/blood*
Bacterial immunity and immunogenesis of normal human salivary IgA and serum IgG2 antiphospholipid autoantibody: a link?

Cheng HM, Sam CK

Immunol Lett, 1990 Oct;26(1):7-10.
PMID: 2276764

The anti-phospholipid antibody (aPL) in 26 heat-inactivated normal human sera (NHS) was tested for IgG subclass in ELISA. The specific antibody in NHS included all four IgG antibody subclasses, as well as IgA. The incidence of IgG subclasses ranged from 50% (13/26) for IgG1 to 92% (24/26) for IgG2. Specific IgA anti-phospholipid antibody (aPL) was detected by ELISA in 38% (28/73) of normal human saliva. The salivary IgA aPL bound preferentially to anionic phospholipids including cardiolipin, phosphatidylserine and phosphatidic acid but not to phosphatidylcholine or sphingomyelin. Unlike aPL in normal human sera, aPL in saliva was predominantly not associated with the previously described heat-labile inhibitor of aPL. This may indicate a role of salivary IgA aPL in local immunity by binding to cross-reactive bacterial cell surface components including phospholipids.

Matched MeSH terms: Autoantibodies/analysis; Autoantibodies/immunology*

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