LCMV-specific, class II-restricted cytotoxic T cells in beta 2-microglobulin-deficient mice

Science ◽  
1992 ◽  
Vol 255 (5051) ◽  
pp. 1576-1578 ◽  
Author(s):  
D Muller ◽  
B. Koller ◽  
J. Whitton ◽  
K. LaPan ◽  
K. Brigman ◽  
...  
Keyword(s):  
T Cells ◽  
Cytotoxic T Cells ◽  
Class Ii ◽  
Specific Class ◽  
Beta 2 ◽  
Beta 2 Microglobulin ◽  
Deficient Mice

scholarly journals Most gamma delta T cells develop normally in beta 2-microglobulin-deficient mice.

1992 ◽  
Vol 89 (2) ◽  
pp. 653-657 ◽  
Author(s):  
I. Correa ◽  
M. Bix ◽  
N. S. Liao ◽  
M. Zijlstra ◽  
R. Jaenisch ◽  
...  
Keyword(s):  
T Cells ◽  
Gamma Delta T Cells ◽  
Gamma Delta ◽  
Beta 2 ◽  
Beta 2 Microglobulin ◽  
Deficient Mice

scholarly journals Activation of virus-specific major histocompatibility complex class II-restricted CD8+ cytotoxic T cells in CD4-deficient mice

1995 ◽  
Vol 25 (4) ◽  
pp. 1109-1112 ◽  
Author(s):  
Mirjam H. M. Heemskerk ◽  
Marco W. Schilham ◽  
Henriette M. Schoemaker ◽  
Gerrit Spierenburg ◽  
Willy J. M. Spaan ◽  
...  
Keyword(s):  
T Cells ◽  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Cytotoxic T Cells ◽  
Class Ii ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Deficient Mice

Theiler's virus infection of beta 2-microglobulin-deficient mice.

1993 ◽  
Vol 67 (1) ◽  
pp. 589-592 ◽  
Author(s):  
L Fiette ◽  
C Aubert ◽  
M Brahic ◽  
C P Rossi
Keyword(s):  
Virus Infection ◽  
Theiler's Virus ◽  
Beta 2 ◽  
Beta 2 Microglobulin ◽  
Deficient Mice

Virus-specific HLA Class II-restricted Cytotoxic T Cells

1986 ◽  
pp. 187-192 ◽  
Author(s):  
Steven Jacobson ◽  
William E. Biddison
Keyword(s):  
T Cells ◽  
Cytotoxic T Cells ◽  
Class Ii ◽  
Hla Class Ii

scholarly journals HLA-DR4-IE chimeric class II transgenic, murine class II-deficient mice are susceptible to experimental allergic encephalomyelitis.

1996 ◽  
Vol 183 (6) ◽  
pp. 2635-2644 ◽  
Author(s):  
K Ito ◽  
H J Bian ◽  
M Molina ◽  
J Han ◽  
J Magram ◽  
...  
Keyword(s):  
T Cells ◽  
Autoimmune Diseases ◽  
Mhc Class Ii ◽  
Experimental Allergic Encephalomyelitis ◽  
Class Ii ◽  
Antigen Binding ◽  
Allergic Encephalomyelitis ◽  
Alpha Beta ◽  
Deficient Mice ◽  
Experimental Allergic

To investigate the development of HLA-DR-associated autoimmune diseases, we generated transgenic (Tg) mice with HLA-DRA-IE alpha and HLA-DRB1*0401-IE beta chimeric genes. The transgene-encoded proteins consisted of antigen-binding domains from HLA-DRA and HLA-DRB1*0401 molecules and the remaining domains from the IE(d)-alpha and IE(d)-beta chains. The chimeric molecules showed the same antigen-binding specificity as HLA-DRB1*0401 molecules, and were functional in presenting antigens to T cells. The Tg mice were backcrossed to MHC class II-deficient (IA beta-, IE alpha-) mice to eliminate any effect of endogenous MHC class II genes on the development of autoimmune diseases. As expected, IA alpha beta or IE alpha beta molecules were not expressed in Tg mice. Moreover, cell-surface expression of endogenous IE beta associated with HLA-DRA-IE alpha was not detectable in several Tg mouse lines by flow cytometric analysis. The HLA-DRA-IE alpha/HLA-DRB1*0401-IE beta molecules rescued the development of CD4+ T cells in MHC class II-deficient mice, but T cells expressing V beta 5, V beta 11, and V beta 12 were specifically deleted. Tg mice were immunized with peptides, myelin basic protein (MBP) 87-106 and proteolipid protein (PLP) 175-192, that are considered to be immunodominant epitopes in HLA-DR4 individuals. PLP175-192 provoked a strong proliferative response of lymph node T cells from Tg mice, and caused inflammatory lesions in white matter of the CNS and symptoms of experimental allergic encephalomyelitis (EAE). Immunization with MBP87-106 elicited a very weak proliferative T cell response and caused mild EAE. Non-Tg mice immunized with either PLP175-192 or MBP87-106 did not develop EAE. These results demonstrated that a human MHC class II binding site alone can confer susceptibility to an experimentally induced murine autoimmune disease.

scholarly journals Blockade of transgenic gamma delta T cell development in beta 2-microglobulin deficient mice.

1992 ◽  
Vol 11 (1) ◽  
pp. 25-31 ◽  
Author(s):  
P. Pereira ◽  
M. Zijlstra ◽  
J. McMaster ◽  
J.M. Loring ◽  
R. Jaenisch ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Development ◽  
Cell Development ◽  
Gamma Delta ◽  
Beta 2 ◽  
Beta 2 Microglobulin ◽  
Gamma Delta T Cell ◽  
Deficient Mice

scholarly journals Beta 2-microglobulin-, CD8+ T-cell-deficient mice survive inoculation with high doses of vaccinia virus and exhibit altered IgG responses.

1992 ◽  
Vol 89 (13) ◽  
pp. 6070-6074 ◽  
Author(s):  
M. K. Spriggs ◽  
B. H. Koller ◽  
T. Sato ◽  
P. J. Morrissey ◽  
W. C. Fanslow ◽  
...  
Keyword(s):  
T Cell ◽  
Vaccinia Virus ◽  
Cd8 T Cell ◽  
Beta 2 ◽  
High Doses ◽  
Beta 2 Microglobulin ◽  
Deficient Mice

scholarly journals Reduced Incidence and Delayed Onset of Diabetes in Perforin-deficient Nonobese Diabetic Mice

1997 ◽  
Vol 186 (7) ◽  
pp. 989-997 ◽  
Author(s):  
David Kägi ◽  
Bernhard Odermatt ◽  
Peter Seiler ◽  
Rolf M. Zinkernagel ◽  
Tak W. Mak ◽  
...  
Keyword(s):  
T Cells ◽  
Autoimmune Diabetes ◽  
Cytotoxic T Cells ◽  
Disease Onset ◽  
Spontaneous Diabetes ◽  
Cell Loss ◽  
Β Cell ◽  
Nonobese Diabetic ◽  
Nonobese Diabetic Mice ◽  
Deficient Mice

To investigate the role of T cell–mediated, perforin-dependent cytotoxicity in autoimmune diabetes, perforin-deficient mice were backcrossed with the nonobese diabetes mouse strain. It was found that the incidence of spontaneous diabetes over a 1 yr period was reduced from 77% in perforin +/+ control to 16% in perforin-deficient mice. Also, the disease onset was markedly delayed (median onset of 39.5 versus 19 wk) in the latter. Insulitis with infiltration of CD4+ and CD8+ T cells occurred similarly in both groups of animals. Lower incidence and delayed disease onset were also evident in perforin-deficient mice when diabetes was induced by cyclophosphamide injection. Thus, perforin-dependent cytotoxicity is a crucial effector mechanism for β cell elimination by cytotoxic T cells in autoimmune diabetes. However, in the absence of perforin chronic inflammation of the islets can lead to diabetogenic β cell loss by less efficient secondary effector mechanisms.

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