Anti-CD72 monoclonal antibody, clone Bu40

The CD5(+)B lymphocyte (B1a) population is known to be involved in most immune responses to microorganism Tl antigens. Moreover, xid mice deficient for immune responses against Tl-2 antigens are known to lack the B1a population, suggesting a role for B1a cells in Tl-2 immune responses. We previously established that the oligosaccharide human blood group A antigen stimulated murine Tl-2 immune responses. In this work, we show that the frequency of anti-A-secreting hybridomas was higher in mice with larger splenic B1a populations and that in vivo anti-CD5 treatment reduced anti-A immune response without affecting the response against TD RBC antigens. A similar effect was observed by in vitro anti-CD5 treatment of splenocytes. The in vivo anti-CD5 treatment also interfered with the immunization-dependent increase in splenocyte numbers. These results are in agreement with an important role for the B-cell CD5 receptor in the regulation of Tl-2 immune responses possibly mediated by its interaction with the CD72 ligand.

Comparative analysis of association with psoriasis before and after treatment of 53K/H2A and 43K/H2A leukocyte protein markers and parameters of leukocyte population (18 indexes) including concentration of peripheral blood lymphocyte subpopulations as markers of the immune status revealed advantages of the former method of patient monitoring for the evaluation of treatment efficacy. The method showed 100% sensitivity and correlation with the dynamics of clinical symptoms. A significant correlation of 53K/H2A parameter with blood content of CD3(+), CD4(+), CD8(+), and CD72(+) lymphocytes was established.