B—B cell interaction involved in polyclonal B cell activation is restricted by I-A but not by I-E molecules

Abstract

We have previously demonstrated that the class II MHC restricted B-B cell interaction is involved in the polyclonal differentiation of unprimed murine B cells into IgM-producing cells induced by a T cell-derived lymphokine B151-TRF2 or bacterial LPS. The present study has addressed the question of whether I-A and/or I-E molecules function as restriction elements for the B-B cell interaction. The results revealed that (B10 x B10.BR)F1(H-2b/k) B cells could be separated into I-Ab- and 1-Ak-restricted subpopulations by their ability to bind to B10(H-2b) or B10.BR(H-2k) B cell monolayers, whereas an I-E-restricted F1 B cell population was not obtained. Moreover, B10-derived B cells isolated from (B10 + B10.BR) - (B10 x B10.BR)F1 but not from B10 - (B10 x B10.BR)F1 radiation-induced bone marrow chimeras acquired newly the ability to co-operate with mitomycin C-treated auxilary B cells expressing I-Ak but not I-Ek molecules. Thus, these results indicate that I-E molecules, unlike I-A molecules, do not serve as restriction elements for the B-B cell interaction, and that I-A and I-E molecules on B cells play functionally disparate roles in the activation of polyclonal B cells.

Autoimmune syndrome after induction of neonatal tolerance to I‐E antigens

“…The I-E antigens ability to mediate allogeneic cooperation in vivo is in agreement with the full blown cGVHD induced through an isolated difference in I-E antigens [34,351. All these results are difficult to reconcile with the reported differential nature of the signals mediated by I-A and I-E molecules in the T-B interactions [25,26,36]. But, in agreement with the results presented in this report, it has been recently shown that the immune responses in I-A-I-E+ and in I-A+ I-E-mice are functionally equivalent [ 121.…”

Evaluation of the functional equivalence of major histocompatibility complex class II A and E complexes.

“…In addition, mice which express E molecules are generally more susceptible to certain parasitic infections, provoking the speculation that a response restricted by this isotype can suppress the "clearing" response normally restricted by A molecules (8). Fourth and finally, there is some evidence that A and E molecules differentially mediate B cell interactions, perhaps because of variant signaling properties (9)(10)(11).…”