Correlation between computed conformational properties of cytochromec peptides and their antigenicity in a T-lymphocyte proliferation assay

Biopolymers ◽  
1987 ◽  
Vol 26 (3) ◽  
pp. 373-386 ◽  
Author(s):  
Max Vasquez ◽  
Matthew R. Pincus ◽  
Harold A. Scheraga
Keyword(s):  
T Lymphocyte ◽  
Lymphocyte Proliferation ◽  
Lymphocyte Proliferation Assay ◽  
Proliferation Assay ◽  
T Lymphocyte Proliferation ◽  
Conformational Properties

scholarly journals H-2D control of recovery from Friend virus leukemia: H-2D region influences the kinetics of the T lymphocyte response to Friend virus.

1983 ◽  
Vol 157 (6) ◽  
pp. 1736-1745 ◽  
Author(s):  
W J Britt ◽  
B Chesebro
Keyword(s):  
T Lymphocyte ◽  
Lymphocyte Proliferation ◽  
Lymphocyte Proliferation Assay ◽  
Friend Virus ◽  
Proliferation Assay ◽  
Lymphocyte Response ◽  
T Lymphocyte Proliferation ◽  
Virus Dose ◽  
Kinetics Of

A Friend virus (FV)-specific T lymphocyte proliferation assay was used to compare the T lymphocyte responses of H-2 congenic mice that differed in their ability to recover from FV leukemia after inoculation of high virus doses. Gene(s) of the H-2D region influenced the kinetics of this response such that H-2Db/b homozygous mice were positive 6-8 d earlier than H-2Dd/b mice. This correlated with the Rfv-1, H-2D-linked influence on recovery from FV by these mice, and also appeared to explain the prominent effect of virus dose on recovery incidence. These findings were supported by the ability of passively transferred immune splenic T lymphocytes to induce recovery from leukemia at 6 d after FV inoculation, but not at 16 d. H-2a/a mice were found to be unresponsive in the FV-specific T lymphocyte proliferation assay. This effect mapped to the left of H-2D, possibly in the H-2I region, and may be an in vitro manifestation of the Rfv-2 gene. No evidence for nonspecific immunosuppression of the T lymphocyte response to concanavalin A was observed in any of the H-2 congenic F1 mice studied.

scholarly journals T-lymphocyte-enriched murine peritoneal exudate cells. II. Genetic control of antigen-induced T-lymphocyte proliferation.

1976 ◽  
Vol 143 (3) ◽  
pp. 529-540 ◽  
Author(s):  
R H Schwartz ◽  
W E Paul
Keyword(s):  
Immune Response ◽  
Genetic Control ◽  
B Lymphocytes ◽  
T Lymphocyte ◽  
Lymphocyte Proliferation ◽  
Proliferative Response ◽  
Antibody Responses ◽  
Lymphocyte Proliferation Assay ◽  
Proliferation Assay ◽  
T Lymphocyte Proliferation

The recent introduction of a reliable, T-lymphocyte proliferation assay, which utilizes thioglycollate-induced, nylon wool column-passed, peritoneal exudate lymphocytes from immune mice (PETLES), allowed us to investigate the genetic control of murine immune responses at the T-lymphocyte level. Examination of the blast cells generated in this population 5 days after stimulation with antigen, revealed that 85% of the cells bore the Thy 1 antigen on their surface, whereas only 5% bore immunoglobulin. Thus, the assay can be considered to measure almost exclusively T-lymphocyte function. This assay was used to examine the T-lymphocyte proliferative responses to seven different antigens: poly(Glu60Ala30Tyr10), poly(Glu58Lys38Tyr4), poly-(Tyr,Glu)-poly-D,L-Ala--poly-Lys, poly-(Phe,Glu)-poly-D,L-Ala--poly-Lys, staphylococcal nuclease, lactate dehydrogenase H4, and the BALB/c IgA myeloma protein, TEPC-15. PETLES from a large number of different inbred mouse strains, including H-2 congenic resistant lines and H-2 recombinants, were studied. The strains could be classified as high responders, low responders, or nonresponders to a particular antigen as judged by the magnitude of the T-lymphocyte proliferative response. In every case but one this classification corresponded to the responder status given the strain based on its ability to mount an in vivo antibody response to the same antigen. For two of the antigens, poly-(Tyr,Glu)-poly-D,L-Ala--poly-Lys and TEPC-15, the immune response genes controlling the T-lymphocyte proliferative response were mapped to the K region or I-A subregion of the major histocompatibility complex, as had previously been shown for the control of the antibody responses to these antigens. This tight linkage of the two phenotypic responses very strongly suggests that the same immune response gene controls the expression of both the proliferative and antibody responses. Since there is essentially no contribution from B lymphocytes in the T-lymphocyte proliferation assay, it seems reasonable to conclude that none of the seven immune response genes studied are expressed solely in B lymphocytes.

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