**2.2 B cells**

B cells contribute to antibody production *i.e.* RF and anticyclic citrullinated peptide antibody (ACPA), and other effector roles to entail disease progression [17]. RF and/or ACPA promotes severe bone and joint erosions as the citrullinated proteins aggravate RA progression [18]. B cells are pointedly responsible for regulation of inflammatory response by serving as antigen-presenting cells and releasing

#### **Figure 1.**

*Schematic illustration indicating the key events and signaling cascades involved in RA pathophysiology. Leukocytes infiltrate synovium and stimulate the inflammatory cascade, characterized by cross-talk of SF and macrophages, monocytes, mast cells, dendritic cells, as well as B and T cells. Endothelial cells facilitate angiogenesis. The advanced stage includes hyperplastic synovium, cartilage damage, bone erosion, and systemic consequence. Bone resorption by osteoclasts practically creates bone erosions. The obliteration of the subchondral bone can ultimately lead to the degeneration of the articular cartilage that is a result of reduced osteoblasts and an increase in the number of osteoclasts and synoviocytes.*

pro−/anti-inflammatory cytokines that additionally control T cell differentiation and proliferation, and activation of macrophages [5].
