Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1996 Oct 1;184(4):1279-84.
doi: 10.1084/jem.184.4.1279.

CD5 is a potential selecting ligand for B cell surface immunoglobulin framework region sequences

Affiliations

CD5 is a potential selecting ligand for B cell surface immunoglobulin framework region sequences

R Pospisil et al. J Exp Med. .

Abstract

In rabbits nearly all B lymphocytes express the glycoprotein CD5, in contrast to mice and humans, where only a small proportion of B cells express this molecule (Raman, C., and K.L. Knight. 1992. J. Immunol. 149:3858-3864). CD5+ B cells appear to develop early in ontogeny and be maintained throughout life by self-renewal. The function of CD5 on B cells is still unknown. We showed earlier that "positive" selection occurs during B lymphocyte development in the rabbit appendix. This selection favors B cell expressing surface immunoglobulins with VHa2 structures in the first and third framework regions (Pospisil, R., G.O. Young-Cooper, and R.G. Mage. 1995. Proc. Natl. Acad. Sci. USA. 92:6961-6965). Here we report that F(ab')2 fragments, especially those bearing VHa2 framework region determinants, specifically interact with the B cell-surface glycoprotein CD5. This interaction can be inhibited by anti-CD5 antibodies. Furthermore, immobilized F(ab')2 fragments selectively bind CD5 molecules in appendix cell lysates. Interactions of VH framework region structures with CD5 may affect maintenance and selective expansion of particular B cells and thus contribute to autostimulatory growth of autoimmune or transformed cells.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Immunol Rev. 1994 Feb;137:91-118 - PubMed
    1. Eur J Immunol. 1994 Apr;24(4):812-6 - PubMed
    1. Proc Natl Acad Sci U S A. 1995 Jul 18;92(15):6961-5 - PubMed
    1. Science. 1995 Jul 28;269(5223):535-7 - PubMed
    1. Immunol Today. 1995 Aug;16(8):399-405 - PubMed

MeSH terms

Substances