Genetic control of the content and avidity of hapten-binding B lymphocytes in mouse spleen

Abstract

The content and the avidity curves of IgM-positive spleen B lymphocytes forming rosettes with TNP-SRBCI were compared in C57BL/6 and BALB/c mice (C57BL/6 × BALB/c)F₁ hybrids, as well as F₁ × C57BL/6 and F₁ × BALB/c backcross hybrids. Conjugates of bovine serum albumin with trinitrophenyl. dinitrophenylsulfonic and sulfanilic acids were used as inhibitors (TNP₂₄BSA, DNP₂₃BSA, Sulf₁₇BSA).

The spleen TNP-RFC content in BALB/c mice was 60% higher than in the C57BL/6 strain. F₁ hybrids were intermediate in this respect. F₁ × BALB/c hybrids had on the average 35% more TNP/RFC than F₁ × C57BL/6 mice.

The TNP-RFC inhibition (avidity) curves obtained with TNP₂₄BSA, DNP₂₃BSA and Sulf₁₇BSA were markedly different in BALB/c, C57BL/6 and (BALB/c × C57BL/6)F₁ animals. We conclude that the spleen content and avidity of TNP-RFC in mice are subject to strict genetic control.

Assuming random expression of V (idiotype?) genes, the present results seem to indicate that the content and proportions of groups of B clones are controlled by structural immunoglobulin genes. The simplest control mechanism could be provided by definite quantitative relationships between corresponding groups of V genes.