| First Author | Dal Porto JM | Year | 2002 |
| Journal | J Exp Med | Volume | 195 |
| Issue | 9 | Pages | 1215-21 |
| PubMed ID | 11994427 | Mgi Jnum | J:124415 |
| Mgi Id | MGI:3721487 | Doi | 10.1084/jem.20011550 |
| Citation | Dal Porto JM, et al. (2002) Very low affinity B cells form germinal centers, become memory B cells, and participate in secondary immune responses when higher affinity competition is reduced. J Exp Med 195(9):1215-21 |
| abstractText | To understand the relationship between the affinity of the B cell antigen receptor (BCR) and the immune response to antigen, two lines of immunoglobulin H chain transgenic (Tg) mice were created. H50Gmu(a) and T1(V23)mu(a) mice express mu H chain transgenes that associate with the lambda1 L chains to bind the (4-hydroxy-3-nitrophenyl)acetyl hapten with association constants (K(a)s) of only 1.2 x 10(5) M(-1) and 3 x 10(4) M(-1), respectively. Both lines mounted substantial antibody-forming cell (AFC) and germinal center (GC) responses. H50Gmu(a) Tg mice also generated memory B cells. T1(V23)mu(a) B cells formed AFC and GCs, but were largely replaced in late GCs by antigen-specific cells that express endogenous BCRs. Thus, B lymphocytes carrying BCRs with affinities previously thought to be irrelevant in specific immune responses are in fact capable of complete T cell-dependent immune responses when relieved of substantial competition from other B cells. The failure to observe such B cells normally in late primary responses and in memory B cell populations is the result of competition, rather than an intrinsic inability of low affinity B cells. |
