HLA -A,B,C DRB1,DQBI

HLA‑DQB1 positive means you carry one or more alleles of the HLA‑DQB1 gene, part of the HLA class II system that helps present antigens to immune cells. Certain DQB1 variants (for example those forming HLA‑DQ2 or DQ8) confer genetic susceptibility to conditions like celiac disease and some autoimmune disorders. A positive result indicates increased risk, not a definitive diagnosis.

HLA-DQB1 alleles are linked to autoimmune and immune-mediated diseases including type 1 diabetes, celiac disease, narcolepsy with cataplexy, multiple sclerosis, rheumatoid arthritis, Graves’ disease, systemic lupus erythematosus, pemphigus vulgaris and certain psoriasis subtypes. Specific DQB1 variants (for example DQB1*02, *03:02, *06:02) confer increased susceptibility or protection depending on the condition.

HLA-DRB1 alleles—especially the “shared epitope” variants—are strongly associated with rheumatoid arthritis. These alleles increase susceptibility to RA and are linked to more severe, erosive disease and higher anti-CCP antibody presence. HLA-DRB1 variants are also implicated in other autoimmune conditions (e.g., type 1 diabetes, multiple sclerosis, and lupus), but the strongest association is with rheumatoid arthritis.

HLA-DRB1 stands for Human Leukocyte Antigen DR beta 1. It’s a gene encoding the beta chain of the HLA‑DR major histocompatibility complex class II protein, which presents peptide antigens to CD4+ T cells. Highly polymorphic, DRB1 affects immune responses, transplant compatibility, and susceptibility to several autoimmune diseases such as rheumatoid arthritis.

Ankylosing spondylitis is strongly associated with HLA genes—particularly HLA‑B27. People who carry HLA‑B27 have a much higher risk of developing this inflammatory spinal arthritis; the allele is found in a large majority of patients with the disease though prevalence varies by population. HLA variants are also linked to other autoimmune conditions, but HLA‑B27 and ankylosing spondylitis are the classic example.

HLA‑DQ testing identifies genetic markers linked to celiac disease. Presence of DQ2 and/or DQ8 indicates increased susceptibility but is not diagnostic—many carriers never develop disease. Absence of both makes celiac disease very unlikely. Results must be interpreted with symptoms and serology (tTG‑IgA, total IgA); if concern remains, discuss gastroenterology referral for further evaluation or biopsy.