Monoclonal Antibody Development Targeting CD80/86-CD28 for Autoimmune Diseases

The cluster of differentiation (CD) 80/86 (CD80/86)-CD28 co-stimulatory pathway is required for the proper T cell activation. Therefore, attenuating T cell activation by inhibiting this pathway is a method that can be used to treat autoimmune diseases. Creative Biolabs offers comprehensive monoclonal antibody (mAb) development services to promote autoimmune disease treatment, such as mAbs targeting CD80/86-CD28. Our high-quality services are supported by an experienced team of scientists working with the latest technology.

Short Introduction of CD80/86-CD28

CD28 and CD80 (B7-1)/CD86(B7-2) represent one of the most relevant costimulatory pathways of the Ig family. During the very early stage of T-cell activation, CD28 is expressed on T cells and is ligated by CD80/CD86 which are constitutively expressed on dendritic cells (DCs) and inducible in other professional antigen-presenting cells (APCs) such as B cells and monocytes. CD28 stimulation has been shown to prolong and augment interleukin 2 (IL-2) production from T cells and prevent the development of peripheral immune tolerance.

Fig.1 Co-stimulatory receptor-ligand pairs in the initiation of a T-cell response. (Goronzy, 2008)

CD80/86-CD28 and Autoimmune Diseases

Study has shown that CD28 promotes T-cell proliferation through the induction of IL-2 secretion after binding to CD80 and CD86. Scientists found that in patients with systemic sclerosis (SS), soluble CD28 levels were increased when compared with a healthy person. In addition, higher levels of circulating soluble CD28 were detected in patients with associated autoimmune disorders, such as systemic lupus erythematosus (SLE), Sjogren's syndrome, and polymyositis.

Treatment of Autoimmune Diseases by Blocking CD80/86-CD28

A study found that cytotoxic T-lymphocyte antigen (CTLA) 4-immunoglobulin (Ig) was a good way to inhibit CD28-CD80/CD86 interaction. The theory behind this study is that CTLA4 binds to CD80 and CD86 with greater affinity than to CD28, it can outcompete CD28 and limit T-cell responses. In some models of treatment of autoimmune disease, CTLA-4 Ig treatment prevents autoantibody production, reduces the severity of lupus nephritis, and prolongs survival in mice. CTLA-4 Ig treatment also prevents experimental autoimmune encephalomyelitis (EAE) which was induced by either active immunization or adoptive transfer of activated antigen-specific T cells.

Fig.2 Initial phase of immune activation. (Yee, 2013)

Custom Services of Monoclonal Antibody Development Targeting CD80/86-CD28

With expertise in antibody discovery, Creative Biolabs can provide flexible solutions for your choice. Either stand-alone service or integrated project is both welcome to meet every specific demand. We strive to retain our customers through competitive cost, strong communication, timeliness, and responsive programs. Based on CD80/86-CD28, we offer comprehensive mAb development services aided by our advanced platforms, including but not limited to:

With access to advanced instruments, fit-for-purpose laboratories, and professional knowledge, Creative Biolabs provides customized CD80/86-CD28 mAb development services to meet the needs of our clients. If you are interested in our services, please contact us.

References

1. Goronzy, J. J.; Weyand, C. M. T-cell co-stimulatory pathways in autoimmunity. Arthritis research & therapy. 2008, 10
2. Yee, K. N.; Anselm, M. Costimulatory Pathways: Physiology and Potential Therapeutic Manipulation in Systemic Lupus Erythematosus. Clinical & Developmental Immunology. 2013, 2013: 245928.

For Research Use Only | Not For Clinical Use