scholarly journals Immune response genes controlling responsiveness to major transplantation antigens. Specific major histocompatibility complex-linked defect for antibody responses to class I alloantigens.

1982 ◽  
Vol 155 (1) ◽  
pp. 303-320 ◽  
Author(s):  
G W Butcher ◽  
J R Corvalán ◽  
D R Licence ◽  
J C Howard
Keyword(s):  
Major Histocompatibility Complex ◽  
Antibody Response ◽  
Antibody Responses ◽  
Class I ◽  
Control Analysis ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Transplantation Antigens ◽  
Ir Genes

We have identified two major histocompatibility complex (MHC)-linked Ir genes that control the antibody response made by rats against class I major alloantigens. We have named these genes Ir-RT1Aa and Ir-RT1Ac. These Ir genes determine responsiveness of the immunized animal in a typical codominant fashion. There is no evidence so far for trans-complementation between low-responder haplotypes. Detailed studies of Ir-RT1Aa indicate that it controls the antibody response to at least two distinct alloantigenic determinants on RT1Aa molecules. These class I molecules thus behave like hapten-carrier conjugates when the response against the carrier is under Ir gene control. Analysis of the origin of alloantibody-forming cells in tetraparental radiation chimeras indicates that Ir-RT1Aa must control the provision of effective help to B cells. In many respects therefore, the properties of Ir-RT1Aa are broadly similar to those described for Ir genes controlling antibody responses to conventional antigens. The existence of apparently conventional Ir genes controlling the antibody response to major alloantigens strongly suggest that the processing of these transmembrane molecules by host antigen-presenting cells is a prerequisite for immune induction, and that it is the MHC of the responder rather than that of the allograft to which T helper cells are restricted in alloimmune responses in vivo.

scholarly journals Human Cytomegalovirus US2 Causes Similar Effects on Both Major Histocompatibility Complex Class I and II Proteins in Epithelial and Glial Cells

2003 ◽  
Vol 77 (17) ◽  
pp. 9287-9294 ◽  
Author(s):  
Nagendra R. Hegde ◽  
David C. Johnson
Keyword(s):  
Major Histocompatibility Complex ◽  
Human Cytomegalovirus ◽  
Adenovirus Vector ◽  
Class Ii ◽  
Class I ◽  
Major Histocompatibility ◽  
Biologically Relevant ◽  
Histocompatibility Complex ◽  
In Cells

ABSTRACT The human cytomegalovirus (HCMV) glycoprotein US2 specifically binds to major histocompatibility complex (MHC) class I heavy chain (HC) and class II proteins DRα and DMα, triggering their degradation by proteasomes. Effects of US2 on class II proteins were originally characterized in HCMV- or adenovirus vector-infected U373 astroglioma cells. Here, we have extended characterization of US2-mediated degradation of class II DRα to two other cell lines, including biologically relevant epithelial cells. Comparison of the effects of US2 in cells expressing both class I and II proteins demonstrated only a slight preference for class I HC. Moreover, US2 caused degradation of DRα and DMα when these proteins were expressed by transfection without DRβ, invariant chain (Ii), or DMβ. Therefore, US2 binds to α chains of DR and DM and triggers endoplasmic reticulum degradation without formation of class II DR αβ/Ii or DM αβ complexes. Similar levels of degradation of class II α were observed in cells expressing vastly different amounts of class II, suggesting that cellular factors, other than class II, were limiting. We concluded that US2 has broad effects in a variety of cells that express both class I and II proteins and is relevant to HCMV infection in vivo.

scholarly journals Highly Pathogenic Simian Immunodeficiency Virus mne Variants That Emerge during the Course of Infection Evolve Enhanced Infectivity and the Ability To Downregulate CD4 but Not Class I Major Histocompatibility Complex Antigens

2002 ◽  
Vol 76 (13) ◽  
pp. 6425-6434 ◽  
Author(s):  
Parul G. Patel ◽  
Monica T. Yu Kimata ◽  
Julia E. Biggins ◽  
Joelle M. Wilson ◽  
Jason T. Kimata
Keyword(s):  
Major Histocompatibility Complex ◽  
Simian Immunodeficiency Virus ◽  
Mhc Class I ◽  
Class I ◽  
Major Histocompatibility ◽  
Highly Pathogenic ◽  
Pathogenic Variants ◽  
Histocompatibility Complex ◽  
Immunodeficiency Virus

ABSTRACT The replicative, cytopathic, and antigenic properties of simian immunodeficiency virus (SIV) variants influence its replication efficiency in vivo. To further define the viral properties and determinants that may be important for high-level replication in vivo and progression to AIDS, we compared a minimally pathogenic SIVmne molecular clone with two highly pathogenic variants cloned from late stages of infection. Both variants had evolved greater infectivity than the parental clone due to mutations in nef. Interestingly, a pol determinant in one of the highly pathogenic variants also contributed to its increased infectivity. Furthermore, because replication in vivo may also be influenced by the ability of a virus to evade the cellular immune response of the host, we examined whether the variants were more capable of downregulating surface expression of class I major histocompatibility complex (MHC). Decreased MHC class I expression was not observed in cells infected with any of the viruses. Furthermore, the Nef proteins of the highly pathogenic variants only slightly reduced surface MHC class I expression in transfected cells, although they efficiently downregulated CD4. Together, these data demonstrate that mutations which can enhance viral infectivity, as well as CD4 downregulation, may be important for efficient replication of SIV in the host. However, Nef-mediated reduction of MHC class I expression does not appear to be critical for the increased in vivo replicative ability of highly pathogenic late variants.

scholarly journals Major Histocompatibility Complex Class I Gene Controls the Generation of Gamma Interferon-Producing CD4+and CD8+ T Cells Important for Recovery from Friend Retrovirus-Induced Leukemia

2000 ◽  
Vol 74 (11) ◽  
pp. 5363-5367 ◽  
Author(s):  
Karin E. Peterson ◽  
Michihiro Iwashiro ◽  
Kim J. Hasenkrug ◽  
Bruce Chesebro
Keyword(s):  
T Cells ◽  
Major Histocompatibility Complex ◽  
Mhc Class I ◽  
Gamma Interferon ◽  
Class I ◽  
Major Histocompatibility ◽  
Cell Responses ◽  
Histocompatibility Complex ◽  
Ifn Γ

ABSTRACT Recovery from leukemia induced by Friend virus complex (FV) requires strong CD4+ helper, CD8+ cytotoxic T-lymphocyte, and B-cell responses. The development of these immune responses is dependent on the major histocompatibility complex (MHC) (H-2) genotype of the mouse. InH-2b/b mice, which spontaneously recover from FV-induced erythroleukemia, neutralization of gamma interferon (IFN-γ) in vivo inhibited recovery, which indicated that IFN-γ was a necessary component of the immune response to FV. Furthermore, inH-2b/b mice, high numbers of IFN-γ-producing cells were detected after FV infection, whereas inH-2a/b mice, which have a low-recovery phenotype, only low numbers of IFN-γ-producing cells were detected. Similarly, H-2bm14/b mice, which cannot recover from FV infection due to a point mutation in one allele of theH-2Db gene, also had low numbers of IFN-γ-producing T cells. Surprisingly, this effect was observed for both CD8+ and CD4+ T cells. These findings reveal a novel influence of MHC class I genes on CD4+T-cell responses to viral infection. Furthermore, the influence of MHC class I genotype on the generation of both IFN-γ-producing CD4+ and CD8+ T cells helps explain the major impact of the H-2D gene on recovery from FV disease.

scholarly journals Immune Modulator Adamantylamide Dipeptide Stimulates Efficient Major Histocompatibility Complex Class I-Restricted Responses in Mice

2007 ◽  
Vol 14 (5) ◽  
pp. 538-543 ◽  
Author(s):  
Pablo D. Becker ◽  
Miriam Nörder ◽  
Carlos A. Guzmán ◽  
Saul Grinstein
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Mucosal Vaccine ◽  
Class I ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Adaptive Responses ◽  
Promising Tool ◽  
Histocompatibility Complex

ABSTRACT Adamantylamide l-alanyl-d-isoglutamine (AdDP) is a synthetic adjuvant which belongs to the family of the desmuramyl peptides. AdDP exerts its adjuvant properties when it is administered either by the parenteral or by the mucosal route, leading to the elicitation of strong humoral responses at both the systemic and the mucosal levels. However, very little is known about the effect of AdDP on cellular immunity. Here we demonstrate that AdDP is able to stimulate cellular responses, which are characterized by the release of gamma interferon by CD8+ T cells when they are restimulated with a major histocompatibility complex class I-restricted peptide and strong in vivo lymphocyte-mediated cytotoxic activity. The capacity of AdDP to stimulate the elicitation of both cellular and humoral adaptive responses makes this adjuvant a promising tool for the development of mucosal vaccine formulations.

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