Leishmania Major Infection in Major Histocompatibility Complex Class II-Deficient Mice: CD8+ T Cells Do not Mediate a Protective Immune Response

Immunobiology ◽  
1996 ◽  
Vol 195 (2) ◽  
pp. 243-260 ◽  
Author(s):  
Klaus Erb ◽  
Christine Blank ◽  
Uwe Ritter ◽  
Horst Bluethmann ◽  
Heidrun Moll
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Cd8 T Cells ◽  
Leishmania Major ◽  
Complex Class ◽  
Major Infection ◽  
Histocompatibility Complex ◽  
Deficient Mice

scholarly journals A tumor escape variant that has lost one major histocompatibility complex class I restriction element induces specific CD8+ T cells to an antigen that no longer serves as a target.

1993 ◽  
Vol 178 (3) ◽  
pp. 933-940 ◽  
Author(s):  
S Seung ◽  
J L Urban ◽  
H Schreiber
Keyword(s):  
T Cells ◽  
Major Histocompatibility Complex ◽  
Cell Surface ◽  
Major Histocompatibility Complex Class ◽  
Cd8 T Cells ◽  
Complex Class ◽  
Ctl Response ◽  
Escape Variant ◽  
Histocompatibility Complex

After loss of expression of a major histocompatibility complex class I Kk allele, the escape variant of an immunogenic tumor grows progressively in normal mice. This progressor variant is resistant to killing by cytotoxic T lymphocytes (CTLs) directed against the A and B antigens presented by Kk. Although the variant retains the expression of the Dk allele and is sensitive to CTLs directed against the C antigen presented by Dk, the variant failed to induce CTLs to this antigen in vivo. Instead, the variant induced CD8+ T cells directed to the A antigen. This was shown at the molecular level by T cell receptor beta chain sequence analysis of the responding cells. Further evidence for the presence of A antigen in the variant came from the finding that spleen cells of mice injected intraperitoneally with the variant tumor cells were primed for an anti-A CD8+ CTL response in vivo. Thus, in contrast to other variants that lost a target antigen and induced a CTL response to remaining target antigens, the Kk loss variant continued to induce an immune response to a tumor antigen that is no longer presented on the tumor cell surface. Even though the variant escapes in a single step because an effective CTL response to secondary antigens is prevented, these secondary antigens remain as potential targets of immunotherapy on the variant's cell surface.

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