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Rheumatic diseases, such as rheumatoid arthritis (RA), lupus and multiple sclerosis, are caused by autoimmune responses. While in immune deficiency disorders the immune system fails to elicit the appropriate immune responses, in autoimmune disorders the immune system overresponds against one’s own antigens. This failure to distinguish between self and nonself antigens arises from breach of immune tolerance, the preventative mechanisms the immune system has in place to prevent attacking itself.1 Autoimmunity could affect specific tissues or it could be systemic (lupus). Some diseases such as ankylosing spondylosis are considered both autoimmune as well as inflammatory arthritic diseases.
Rheumatoid arthritis (RA) is an autoimmune disorder characterized by inflammation and damage of the joints throughout the body, including hands and feet and affects about 0.5–1% of the population, being more common among women than men in the United States.2
Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease. It affects multiple organ systems, such as the skin, kidneys, lungs and the central nervous system, by producing autoantibodies.3
Ankylosing spondylosis (AS) is a chronic, progressive inflammatory rheumatic disease of the axial musculoskeletal system caused by multiple genes.4
RA could be divided into two categories:
During inflammation, the amino acid arginine is converted into citrulline by peptidylarginine deaminase (PAD). This process, called citrullination, elicits formation of antibodies, which are almost certain indicators of development of RA within a few years.5 The ACAP positive type is more aggressive than the ACPA negative type.6
The progression of RA occurs gradually, closely following a concatenation of immunological events.7 The process has been divided into five steps as described below:
Genetic factors contribute significantly to RA. In particular, the human leukocyte antigen (HLA) locus accounts for about 50% of genetic predisposition to RA, with a strong involvement of HLA-DRB1, a major histocompatibility complex (MHC) class II molecule, with several HLA-DRB1 alleles implicated across different ethnic populations.6 Other non-HLA susceptibility genes, such as protein-arginine deiminase type 4 (PADI4) and IL-2 receptor subunit α, are also implicated in RA.
SLE is a complex genetic disease with the involvement of multiple genes. HLA class II DRB is also implicated in SLE.3,8
HLA-B27, an MHC class I molecule, has a strong association with AS. HLA-B27 testing is routinely used to screen for AS.4
The dried, unit-sized, preformulated and optimized BD Horizon™ Dri Treg Panel contains markers used for the characterization of FoxP3+ naïve, translational and effector Treg subsets, directly relevant for autoimmune research.
The BD Horizon™ Dri TBNK + CD20 Panel enables efficient characterization of T, B and NK cells.
The BD Horizon™ Dyes and Antibodies are ideal for characterizing immune cells that have few receptors on the surface and their brightness makes it easy to distinguish these dim cells from others in a sample.
