NAA and Systemic Lupus Erythematosus

Natural autoantibodies (NAA) are closely related to the pathogenesis and treatment of systemic lupus erythematosus (SLE). Creative Biolabs is a leading provider of NAA testing and analysis services. We have a team of experienced professionals and an advanced technology platform to provide a full range of NAA services for SLE research.

Description of SLE

SLE is the prototypical systemic autoimmune disease with significant disease. It's characterized by a global loss of self-tolerance with activation of autoreactive T and B cells leading to the production of pathogenic autoantibodies and tissue injury. SLE affects the joints, skin, and blood in over 80% of patients and the kidneys, central nervous system, and cardiopulmonary system in 30%-50% of patients. The primary pathological findings in patients with SLE are those of inflammation, vasculitis, immune complex deposition, and vasculopathy. Immune complexes comprising autoantibody and self-antigen are deposited particularly in the renal glomeruli and mediate a systemic inflammatory response by activating complement or via FcγR-mediated neutrophil and macrophage activation. Activation of complement (C5) results in damage through the formation of membrane attack complex (C5B-9) or the production of allergic toxin and cell activator C5a. Neutrophils and macrophages cause tissue injury by the release of oxidants and proteases.

Fig.1 Autoantibody in SLE. (Han, et al., 2015)Fig.1 Proposed model of autoantibody production in SLE.1

Pathway of SLE

The loss of tolerance to self and the subsequent elevation in serum ANA levels is proposed to be a crucial first step in the development of SLE. The B cells produced are mostly self-reactive and are usually cleared by central tolerance mechanisms in the bone marrow, including receptor editing, deletion, or induced incompetence. These are intrinsic B cell mechanisms that are known to be controlled by B cell antigen receptor signaling thresholds and regulators of the phosphoinositol 3 kinase pathway. In addition, the generation of newborn autoreactive B cells occurs after maturity as a result of somatic high mutations in germinal centers (GCs). It is thought that most of the pathogenic autoantibodies are somatic highly mutated, type-switching IgGs. TA T-box transcription factors (T-BET) also contribute to the production of pathogenic autoantibodies. TLR7 in B cells is also required for spontaneous GC formation and antibody production.

Other mechanisms that may contribute to ANA production include molecular simulation. Similar to B lymphocytes, T cells have a tolerance mechanism that inhibits their own reactivity. Multiple autoimmune-prone strains have demonstrated a requirement for both B and CD4+ T cells for the production of IgG autoantibodies, indicating that loss of T-cell tolerance may play a role in lupus. In SLE, abnormalities in the proximal signaling pathway can lead to changes in T cell tolerance and reactivity. Tfh cells are important for the activation and selection of B cells in GCs. Interestingly, 3 years prior to diagnosis of SLE serum levels of IFN-γ, IL-5 and IL-6 were higher, suggesting their importance in the development of the disease.

Fig.2 Pathogenesis of SLE. (Robinson, Meredyth and Chris, 2022)Fig.2 The main immunological abnormalities associated with the pathology of SLE.2

NAA Services for SLE at Creative Biolabs

SLE Related Products at Creative Biolabs

Target Product Name Cat. No.
dsDNA autoantibody Human dsDNA Autoantibody (IgG) ELISA kit NAK-035
dsDNA autoantibody Human dsDNA Autoantibody (IgG&IgM&IgA) ELISA kit NAK-036
SS-A 60 autoantibody Human SS-A 60 Autoantibody (IgG) ELISA kit NAK-060
SS-A autoantibody Human SS-A Autoantibody (IgG) ELISA kit NAK-061
SSB autoantibody Human SSB Autoantibody (IgG) ELISA kit NAK-007
RNP/Sm autoantibody Human RNP/Sm Autoantibody (IgG) ELISA kit NAK-057
Sm autoantibody Human Sm Autoantibody (IgG) ELISA kit NAK-059
RNP 70 autoantibody Human RNP 70 Autoantibody (IgG) ELISA kit NAK-056
SS-A (Ro), SS-B (La), Sm and RNP/Sm autoantibody Human SS-A (Ro), SS-B (La), Sm, and RNP/Sm Autoantibody (IgG) ELISA kit NAK-039
SS-A (Ro), SS-B (La), Sm RNP/Sm, Scl-70, and Jo-1 autoantibody Human SS-A (Ro), SS-B (La), Sm RNP/Sm, Scl-70, and Jo-1 Autoantibody (IgG) ELISA kit NAK-040
Cardiolipin, Phosphatidyl Serine, Phosphatidyl Inositol and Phosphatidic acid autoantibody Human Cardiolipin, Phosphatidyl Serine, Phosphatidyl Inositol and Phosphatidic acid Autoantibody (IgG&IgM ) ELISA kit NAK-053

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References

  1. Han, Shuhong, et al. "Mechanisms of autoantibody production in systemic lupus erythematosus." Frontiers in immunology 6 (2015): 228.
  2. Robinson, George Anthony, Meredyth G. Ll Wilkinson, and Chris Wincup. "The role of immunometabolism in the pathogenesis of systemic lupus erythematosus." Frontiers in Immunology 12 (2022): 806560.
For Research Use Only | Not For Clinical Use

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