Altered I-J phenotype in E alpha transgenic mice.

AUTOR(ES)

Flood, P M

RESUMO

One of the more intriguing puzzles in immunology is the genetic basis for control of murine T-cell I-J determinants. Molecules bearing I-J determinants (I-J molecules) play a role in information trafficking among immunocompetent cells, probably serving as self-recognition molecules that channel regulatory factors to their appropriate target cells. Although it is clear that I-J polymorphism is influenced by the major histocompatibility complex (MHC), molecular genetic studies provide evidence that an MHC gene does not encode I-J molecules. A possible explanation for this paradox is that I-J molecules are a set of non-MHC-encoded T cell receptors that are directly or indirectly selected for by self-MHC products. One key to resolving the genetic and molecular basis for control of I-J determinants is the identification of the MHC gene(s) involved. Herein, data are presented which show that E alpha transgenic mice express an altered I-J phenotype, providing clear evidence that I region class II genes influence I-J polymorphism. Although further study is required to resolve how class II genes mediate this effect, this is a major piece to the I-J puzzle.

Documentos Relacionados

• Association of I-J determinants with lipomodulin/macrocortin.
• Association of the "major histocompatibility complex subregion" I-J determinant with bioactive glycosylation-inhibiting factor.
• Murine T cell Ia antigens: specificity Iat.46 maps in I-J to I-E chromosomal segment of H-2 complex.
• Use of anti-idiotypic antibodies to identify a receptor for the T-cell I-J determinant.
• Functional association of idiotypic and I-J determinants on the antigen receptor of suppressor T cells.