Ethan A. Lerner
Yale University
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Featured researches published by Ethan A. Lerner.
Immunogenetics | 1980
A Charles JanewayJr.; Ethan A. Lerner; Janine M. Jason; Barry Jones
We have investigated primary and secondary responses of mouse splenic T cells to strong mixed lymphocyte stimulating antigens controlled by theMls locus using MHC-identical mixtures of cells. Our studies show that strong primaryMls-locus specific responses involve recognition of self I-A antigens, since BUdR and light suicide or F1 into parent radiation bone-marrow chimeras both demonstrate a preference of unprimed F1 T cells to respond to Mis-locus antigens associated with one parents MHC antigens. Furthermore, conventional anti-I-A antisera and monoclonal anti-I-A antibody both inhibitMls-locus responses in an MHC-specific manner. Finally, as is typical of T cells responding to I-A antigens or to nominal antigens associated with self I-A,Mlslocus responses are mediated by Lyt-1+, 2− cells. One striking finding in these studies was the very high frequency of cells capable of responding to Mls-locus antigens, the highest being 1/300 splenic T cells. This plus evidence for recruitment during primaryMls-locus responses may account for reports of a lack ofI-A restriction in secondary anti-Mls locus responses to strong Mls-locus antigens, a finding with which we concur. The possibility that these secondary responses between noncongenic strains of mice may be directed at other genetic loci is also discussed. These experiments leave open the question of the biological role of theMls-locus and of the very large number of T cells reactive to it.
Immunogenetics | 1983
Janet Rucker; Mark C. Horowitz; Ethan A. Lerner; Donal B. Murphy
We have produced a monoclonal antibody, Y-7, that reacts with a Qa-2 region-controlled determinant. Cellular and strain distribution analyses, coupled with quantitative variation in the amount of Y-7 antigen expressed among strains, provide overwhelming evidence that Y-7 reacts with the Qa-2a determinant. The determinant detected by Y-7 is differentially expressed in T and B lymphocytes in a strain specific manner. Y-7 reacts with the majority of T lymphocytes (> 95%) and approximately one-half of B lymphocytes in certain strains (++ strains), and with the majority of T lymphocytes (> 95%) and no B lymphocytes in other strains (+ strains). T lymphocytes in + strains express approximately three fold less of the Y-7 determinant than T lymphocytes from ++ strains. In addition, we show that the Y-7 determinant is expressed in approximately one-third to one-half of Lyb-3−, 5− B lymphocytes. Possible mechanisms determining quantitative and qualitative variation in the expression of the Y-7 determinant in T and B lymphocytes are discussed.
Archive | 1992
Ethan A. Lerner; R. Rox Anderson; Michael R. Lerner
Archive | 1995
Michael R. Lerner; Ethan A. Lerner
Archive | 1991
Michael R. Lerner; Ethan A. Lerner
Archive | 1993
Michael R. Lerner; Channa K. Jayawickreme; Ethan A. Lerner
Arthritis & Rheumatism | 1982
Ethan A. Lerner; Michael R. Lerner; John A. Hardin; Charles A. Janeway; Joan A. Steitz
Archive | 1994
Michael R. Lerner; Channa K. Jayawickreme; Ethan A. Lerner
Archive | 1981
Ethan A. Lerner; Michael R. Lerner
Archive | 1991
Michael R. Lerner; Ethan A. Lerner