Rheumatoid Arthritis antibodies

and ELISA kits, proteins related to Rheumatoid Arthritis.

Introduction to Rheumatoid Arthritis

Rheumatoid Arthritis (RA) is a chronic autoimmune disorder that primarily affects the joints, leading to inflammation, pain, and eventual joint damage. Unlike ordinary wear-and-tear arthritis, RA occurs when the immune system mistakenly attacks the body’s own tissues, particularly the synovium—the lining of the membranes surrounding the joints. This persistent inflammation can result in swelling, stiffness, and reduced mobility, significantly impacting daily life. Beyond joint issues, RA can also affect other organs, including the skin, eyes, and cardiovascular system. Advances in RA research are increasingly focusing on the role of specific antibodies that drive the autoimmune response. By understanding these antibodies, scientists aim to develop targeted therapies that can more effectively manage symptoms, slow disease progression, and improve the quality of life for those living with Rheumatoid Arthritis.

Rheumatoid Arthritis biomarkers

A00101

Anti-IL-1 beta/IL1B Antibody Picoband®, Z-LLSD-FMK or Z-YVAD-FMK inhibited GSDMD activation or pyroptosis induced by LPS + nigericin in BMDMs. BMDMs were primed with LPS for...

RP1080

Anti-Osteopontin/SPP1 Antibody Picoband®, Deciphering the complex interactions among multiple cell lineages in the fibrotic microenvironment of LFH. (A) Circos plots showing potential in...

M00775

Anti-MMP3 Rabbit Monoclonal Antibody, LRRK2-IN-1 suppresses the IL-1β-induced inflammation and catabolism and induces anabolism without causing the inhibition of chondrocyte viab...

Protein Name	Gene Name	Function
C-Reactive Protein (CRP)	CRP	Acute-phase reactant, indicates inflammation
Tumor Necrosis Factor-alpha (TNF-α)	TNF	Promotes inflammation and joint destruction
Interleukin-6 (IL-6)	IL6	Mediates inflammation and immune response
Interleukin-1 beta (IL1B)	IL1B	Pro-inflammatory cytokine involved in joint destruction
Matrix Metalloproteinase-3 (MMP3)	MMP3	Degrades extracellular matrix components
Vascular Endothelial Growth Factor (VEGF)	VEGFA	Promotes angiogenesis in inflamed joints
Anti-Cyclic Citrullinated Peptide (Anti-CCP)	PTPN22	Autoantibody against citrullinated proteins
Osteoprotegerin	TNFRSF11B	Regulates bone resorption
Serum Amyloid A (SAA)	SAA1	Acute-phase reactant, pro-inflammatory
S100 Calcium Binding Protein A12 (S100A12)	S100A12	Mediates inflammatory responses
Interferon-gamma (IFN-γ)	IFNG	Activates macrophages and promotes inflammation
Intercellular Adhesion Molecule 1 (ICAM1)	ICAM1	Facilitates leukocyte adhesion and migration
Osteopontin	SPP1	Involved in bone remodeling and inflammation
Prolactin	PRL	Modulates immune response
CD64	FCGR1A	Marker of activated macrophages
Fibrinogen	FGG	Involved in clot formation, elevated in inflammation
Complement C3	C3	Part of the complement system, involved in immune response
CCL5 (RANTES)	CCL5	Chemokine involved in recruiting immune cells

Important Mechanisms

Autoimmune Mechanisms in Rheumatoid Arthritis

Rheumatoid Arthritis (RA) is fundamentally an autoimmune disorder, where the body's immune system mistakenly attacks its own joint tissues. Central to this autoimmune response are autoantibodies such as rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPAs), which target specific proteins in the synovial fluid of joints. T cells, particularly CD4+ subsets, play a pivotal role by orchestrating the inflammatory response, promoting the activation of B cells, and sustaining the chronic inflammation characteristic of RA. Additionally, dysregulation of immune checkpoints and the presence of pro-inflammatory cytokines contribute to the perpetuation of the autoimmune cycle. Understanding these autoimmune mechanisms is crucial for developing targeted therapies that can modulate the immune response, reduce inflammation, and prevent joint destruction in RA patients.

Pro-Inflammatory Cytokines in Rheumatoid Arthritis

Pro-inflammatory cytokines are key mediators in the pathogenesis of Rheumatoid Arthritis, driving the inflammatory cascade that leads to joint damage. Tumor Necrosis Factor-alpha (TNF-α) and Interleukin-6 (IL-6) are among the most significant cytokines implicated in RA. TNF-α promotes the recruitment of inflammatory cells to the synovium, stimulates the production of other cytokines, and induces the expression of adhesion molecules, facilitating further immune cell infiltration. IL-6 contributes to the acute phase response, B cell maturation, and the differentiation of T cells, exacerbating the inflammatory environment. Therapeutic agents targeting these cytokines, such as TNF inhibitors and IL-6 receptor antagonists, have revolutionized RA treatment by effectively reducing inflammation and slowing disease progression. Ongoing research continues to explore additional cytokine pathways to enhance therapeutic options and improve patient outcomes.