A. Tumor necrosis factor (TNF) primary function in the immune system is to manipulate T cell responses in reducing autoimmune diseases, regulating immune cell functions, and signaling specific responses (Croft, 2009). TFN has 19 ligands with structural and functional similarities and 30 receptors [4]. The interactions between TNF and its receptor, TNFR, involve in T lymphocytes response to other cells by crosstalk [4]. Most TNF ligands are type II transmembrane proteins with cleaved or non-cleaved extracellular domain (Bremer, 2013). They are characterized as hallmark structure or TNF homology domain (THD) and get produced by many cell types [3]. CD70 is one of the TNF superfamily that is a ...view middle of the document...
The activation of B lymphocytes through T lymphocytes interaction allows B lymphocytes proliferation and differentiation. B cells proliferate and differentiate into plasma cells and memory B cells by CD40 signals (Benson, et al, 2006). CD40 and CD95 are important for B cells to trigger an immune response without autoimmunity [1]. One study showed that B lymphocytes with CD95 expressed apoptosis could be rescued by early CD40 stimulation [1]. Also, isotope switching and memory B cells occurred through the ligation of CD40 by CD154 on T cell [1]. CD40 stimulations through T cells allow B cells proliferation, differentiation, isotype switching, humoral memory cells, and prevent apoptosis.
C. Type I interferons, IFN-α and IFN-β, are antiviral mediators that involve in the innate immunity to non-viral pathogens. IFNs are monomers that compose of two subunits, which associate with JAKs and TYKs (Uddin, et al, 2004). The activation of JAKs results in signal transduction and activate transcription, which lead to IFN-stimulated gene factor 3 (ISGF3) [6]. Once ISGF3 is in the nucleus and binds to IFN-stimulated response elements to begin DNA transcription [6]. A recent study on type I interferon indicated that they stimulated B cells differentiation into plasma cells, supported cytotoxicity, and produced cytokines to pathogen-induced apoptosis (Bogdan, et al, 2004). Also, IFN-α...