Role of conserved regions of class I MHC molecules in the activation of CD8+ cytotoxic T lymphocytes by peptide and purified cell-free class I molecules

1993 ◽  
Vol 5 (9) ◽  
pp. 1129-1138 ◽  
Author(s):  
Toshiyuki Takeshita ◽  
Steven Kozlowski ◽  
Richard D. England ◽  
Richard Brower ◽  
Jonathan Schneck ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Cytotoxic T Lymphocytes ◽  
Class I ◽  
Class I Mhc ◽  
Mhc Molecules ◽  
Conserved Regions

scholarly journals Role of  3 domain of class I MHC molecules in the activation of high- and low-avidity CD8+ CTLs

2007 ◽  
Vol 19 (12) ◽  
pp. 1413-1420 ◽  
Author(s):  
I. M. Belyakov ◽  
S. Kozlowski ◽  
M. Mage ◽  
J. D. Ahlers ◽  
L. F. Boyd ◽  
...  
Keyword(s):  
Class I ◽  
Class I Mhc ◽  
Mhc Molecules

scholarly journals Use of synthetic peptides of influenza nucleoprotein to define epitopes recognized by class I-restricted cytotoxic T lymphocytes.

1987 ◽  
Vol 165 (6) ◽  
pp. 1508-1523 ◽  
Author(s):  
J Bastin ◽  
J Rothbard ◽  
J Davey ◽  
I Jones ◽  
A Townsend
Keyword(s):  
T Cells ◽  
T Lymphocytes ◽  
Infected Cell ◽  
Cytotoxic T Lymphocytes ◽  
Synthetic Peptides ◽  
Class Ii ◽  
Cytotoxicity Assay ◽  
Class I ◽  
Class I Mhc

The conserved epitopes of influenza nucleoprotein (NP) recognized by class I MHC-restricted CTL from CBA (H-2k) and C57BL/10 (H-2b) mice have been defined in vitro with synthetic peptides 50-63 and 365-379, respectively. Two Db-restricted clones were described that recognize different epitopes on peptide 365-379. Finally, the recognition of complete NP was shown to be approximately 200-fold less efficient than peptide in the cytotoxicity assay. These phenomena are closely related to results with class II-restricted T cells and they strengthen the hypothesis that influenza proteins are degraded in the infected cell before recognition by class I-restricted CTL.

Accessory Cell Requirements for Saponin Adjuvant-Induced Class I MHC Antigen-Restricted Cytotoxic T-Lymphocytes

1994 ◽  
Vol 154 (2) ◽  
pp. 393-406 ◽  
Author(s):  
Jia-Yan Wu ◽  
Bonnie H. Gardner ◽  
Nicholas N. Kushner ◽  
Lu-Ann M. Pozzi ◽  
Charlotte R. Kensil ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Cytotoxic T Lymphocytes ◽  
Class I ◽  
Accessory Cell ◽  
Class I Mhc ◽  
Mhc Antigen

scholarly journals Induction of tumor-specific CD8+ cytotoxic T lymphocytes from naïve human T cells by using Mycobacterium-derived mycolic acid and lipoarabinomannan-stimulated dendritic cells

2019 ◽  
Vol 68 (10) ◽  
pp. 1605-1619 ◽  
Author(s):  
Yuji Tomita ◽  
Eri Watanabe ◽  
Masumi Shimizu ◽  
Yasuyuki Negishi ◽  
Yukihiro Kondo ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Lymphocytes ◽  
Cytotoxic T Lymphocytes ◽  
Mycolic Acid ◽  
Class I ◽  
Tumor Control ◽  
Class I Mhc ◽  
Ctl Induction ◽  
Tolerogenic Dcs

Abstract The main effectors in tumor control are the class I MHC molecule-restricted CD8+ cytotoxic T lymphocytes (CTLs). Tumor-specific CTL induction can be regulated by dendritic cells (DCs) expressing both tumor-derived epitopes and co-stimulatory molecules. Immunosuppressive tolerogenic DCs, having down-regulated co-stimulatory molecules, are seen within the tumor mass and can suppress tumor-specific CTL induction. The tolerogenic DCs expressing down-regulated XCR1+CD141+ appear to be induced by tumor-derived soluble factors or dexamethasone, while the immunogenic DCs usually express XCR1+CD141+ molecules with a cross-presentation function in humans. Thus, if tolerogenic DCs can be reactivated into immunogenic DCs with sufficient co-stimulatory molecules, tumor-specific CD8+ CTLs can be primed and activated in vivo. In the present study, we converted human tolerogenic CD141+ DCs with enhanced co-stimulatory molecule expression of CD40, CD80, and CD86 through stimulation with non-toxic mycobacterial lipids such as mycolic acid (MA) and lipoarabinomannan (LAM), which synergistically enhanced both co-stimulatory molecule expression and interleukin (IL)-12 secretion by XCR1+CD141+ DCs. Moreover, MA and LAM-stimulated DCs captured tumor antigens and presented tumor epitope(s) in association with class I MHCs and sufficient upregulated co-stimulatory molecules to prime naïve CD3+ T cells to become CD8+ tumor-specific CTLs. Repeat CD141+ DC stimulation with MA and LAM augmented the secretion of IL-12. These findings provide us a new method for altering the tumor environment by converting tolerogenic DCs to immunogenic DCs with MA and LAM from Mycobacterium tuberculosis.

scholarly journals A subpopulation of mouse cytotoxic T lymphocytes recognizes allogeneic H-2 class I antigens in the context of other H-2 class I molecules.

1991 ◽  
Vol 174 (1) ◽  
pp. 15-19 ◽  
Author(s):  
F Kievits ◽  
P Ivanyi
Keyword(s):  
T Lymphocytes ◽  
Cytotoxic T Lymphocytes ◽  
Class I ◽  
Target Antigen ◽  
Single Class ◽  
Mhc Molecules ◽  
Histocompatibility Complex ◽  
Precursor Frequency ◽  
Lines Of Evidence

Recently, independent lines of evidence strongly suggested that peptides derived from one foreign major histocompatibility complex (MHC) molecule bound to another MHC molecule can give rise to multiple composite MHC complexes that are able to stimulate allo-(xeno)-reactive T cells. In this study, we describe that in vivo immunization of mice with cells mismatched with the recipient for a single class I antigen results in the induction of CD8+ cytotoxic T lymphocytes (CTL) specific for allogeneic class I locus products (Dd, Kd, Dq) in the context of other class I molecules (Ks, Kd, Kk) present on stimulator cells. Evidently, the target antigen for these class I-restricted alloreactive CTL is not the native class I molecule but peptides derived from endogenous processing of allogeneic class I products presented by class I molecules. Using a combination of limiting dilution and split-well analyses, we estimated for Kk-restricted Dq-specific alloreactive CTL a precursor frequency (CTLpf) that was approximately 10 times lower than the CTLpf for "classical" nonrestricted Dq-specific alloreactive CTL. These data suggest that H-2 class I peptides presented by intact H-2 class I molecules are allostimulatory, supporting the concept that the capacity for presentation of MHC peptides by MHC molecules constitutes a part of the allogeneic immune response.

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