Biomedical subjects

M E Sunday

Publications and source records attributed to M E Sunday.

57 records · Page 4Linked to original sources

PubMed1981

Hapten-specific T cell response to 4-hydroxy-3-nitrophenyl acetyl. X. Characterization of distinct T cell subsets mediating cutaneous sensitivity responses.

NP-O-Succinimide-induced cutaneous sensitivity (CS) responses can be adoptively transferred by NP-primed lymphoid cells into naive K-, I-, or D-compatible recipients. The distinct fine specificities of I- versus D-restricted T cell clones from various strains of mice suggested that presence of different idiotypic receptors on these T cell subsets. We now demonstrate that NP-O-Su immune lymphoid cells are composed of 2 T cell subsets with distinct antigen recognition patterns, as well as different Lyt 2 phenotypes. Thus, I-restricted cells respond to NP-coupled to a protein carrier but not to NP-coupled cells, whereas D-restricted clones react to NP-cells, but not to NP-protein conjugates.

Animals↗

PubMed1980

Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. VI. Evidence for different T cell receptors in cells that mediate H-21-restricted and H-2D-restricted cutaneous sensitivity responses.

We have previously shown that cross-reactive sensitivity (CS) responses induced by 4-hydroxy-3-nitrophenyl acetyl-O-succinimide (NP-O-Su) and elicited by its 5-iodo analogue, 4-hydroxy-5-iodo-3-nitrophenyl acetyl-O-succinimide were observed in strains of mice possessing the Igh-1b allotype, but not in strains bearing allotypes Igh-1c or Igh-1j. These CS responses are mediated by T cells and can be transferred to naive recipients that are homologous at either the H-2K, H-2I, or H-2D regions of the major histocompatibility complex. We now extend our analysis of cross-reactive 4-hydroxy-3-nitrophenyl-acetyl (NP)-induced CS responses to inbred strains of mice expressing additional Igh-1 allotypes. In contrast to NP-induced delayed-type hypersensitivity responses, which only display 4-hydroxy-5-iodo-3-nitrophenyl acetyl (NIP) cross-reactivity in Igh-1b-bearing mice, cross-reactive CS responses can also be elicited in NP-primed mice carrying the Igh-1d, Igh-1e, or Igh-1f allotypes. Moreover, cross-reactive NP-induced CS responses could be transferred by NP-O-Su-primed lymph node cells from the AKR (Igh-1d) strain, into naive recipients homologous at the H-2D region, but only non-cross-reactive NP responses could be transferred into strains homologous at the H-2I region. Furthermore, the lack of cross-reactivity in the Igh-1j-bearing C3H strain was not the result of an inability of these mice to recognize NP in association with H-2K/D products, because NP-O-Su-primed cells from C3H donors transferred NP-specific CS responses into both H-2D and H02I homologous recipients. The results are discussed with respect to the nature of the T cell receptors that control NP responses.

Animals↗

PubMed1980

Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl.

The primary anti-(4-hydroxy-3-nitrophenyl)acetyl (NP) antibody response is known to have a heteroclitic fine specificity, i.e., anti-NP antibodies bind (4-hydroxy-5-iodo-3-nitrophenyl)acetyl (NIP) with greater affinity than NP itself. Past studies of NP-specific DTH responses and NP-specific T cell-mediated suppression have demonstrated sharing of fine specificity patterns and idiotypic structure between receptors on NP-specific T cells and anti-NP antibodies. We now analyze the fine specificity of NP-specific cutaneous sensitivity (CS) reactions to NP-O-succinimide (NP-O-Su) and NIP-O-succinimide (NIP-O-Su). The specificity of these responses is shown to be controlled by genes in the Igh gene complex. Cross-reactive CS responses induced by NP-O-Su elicited by NIP-O-Su were observed in strains of mice possessing the Igh-1b allotype but not in strains bearing the Igh-1c or Igh-1j allotypes. The CS reactivity could be adoptively transferred to naive recipients, and the ability of transfer CS reactivity was T cell dependent. In contrast to the genetic requirement for I-A region homology to adoptively transfer DTH reactions, compatibility at either the H-2K, H-21, or H-2D regions was sufficient to transfer NP-specific CS reactivity to naive recipients. Furthermore, in contrast to DTH responses, cyclophosphamide pretreatment was not required to induce CS responsiveness. Thus, the specificity of NP-O-Su-induced CS responses is controlled by both H-2- and Igh-linked genes.

Animals↗