Isoforms of the nonclassical class I MHC antigen H2-Q5 are enriched in brain and encode Qdm peptide

It has been shown that peripheral-blood mononuclear leukocytes (MNL) are responsible for transfusion-induced alloimmunization to donor major histocompatability complex (MHC) antigens. However, it is not known which subset of MNL is responsible for this immune response. Because elimination of class-II MHC antigen-positive passenger leukocytes effectively prolongs the survival of allografts, it has been hypothesized that class-II positive MNL are responsible for immunizing transfusion recipients to donor MHC antigens. To test this hypothesis, two different approaches were used. First, we compared the alloantigenicity of BALB/c mice (H-2d) peripheral blood MNL before and after depletion of class-II positive cells. CBA mice (H-2k) were used as transfusion recipients. Antibody development to donor class-I H-2 antigens was determined by flow cytometry and enzyme-linked immunoassay. After four weekly transfusions of MNL depleted for class-II positive cells, only 25% of recipient mice developed antibodies to donor H-2d antigens. In contrast, all mice transfused with control MNL became immunized. Second, we studied the alloantigenicity of peripheral MNL from C57BL/6 mice (H-2b) with homozygous deficiency of class-II MHC molecules in H-2 disparate recipient mice. After transfusions with class-II MHC molecule-deficient MNL, 0% of BALB/c, 40% of C57BR, and 25% of CBA-recipient mice developed antibodies to donor H-2b antigen. All control recipient mice were immunized. The antibody activities of the controls were also higher than those in the treatment group who became immunized. Thus, our study shows that class-II MHC antigen-positive MNL play a significant role in transfusion-induced alloimmunization to donor class-I MHC antigens. The results also support the hypothesis that direct antigen presentation by donor class-II positive MNL to the immune system of transfusion recipients is critical for the initiation of humoral immune response to donor MHC antigens.

Download Full-text

Induction of Tolerance Toward Rat Cardiac Allografts by Treatment With Allochimeric Class I MHC Antigen And FTY7201

Transplantation Journal ◽

10.1097/00007890-199711270-00006 ◽

1997 ◽

Vol 64 (10) ◽

pp. 1407-1414 ◽

Cited By ~ 26

Author(s):

Shih-Chieh Chueh ◽

Ling Tian ◽

Min Wang ◽

Mou-Er Wang ◽

Stanislaw M. Stepkowski ◽

...

Keyword(s):

Class I ◽

Class I Mhc ◽

Cardiac Allografts ◽

Mhc Antigen ◽

Induction Of Tolerance

Download Full-text

TRANSFUSION OF DONOR CLASS I MHC ANTIGEN PRIOR TO KINDNEY TRANSPLANTATION IN DOGS

Transplantation Journal ◽

10.1097/00007890-198605000-00019 ◽

1986 ◽

Vol 41 (5) ◽

pp. 648-649 ◽

Cited By ~ 3

Author(s):

&NA;

Keyword(s):

Class I ◽

Class I Mhc ◽

Mhc Antigen

Download Full-text

Depletion of CD8+ cells in human thymic medulla results in selective immune deficiency.

Journal of Experimental Medicine ◽

10.1084/jem.170.6.2177 ◽

1989 ◽

Vol 170 (6) ◽

pp. 2177-2182 ◽

Cited By ~ 48

Author(s):

C M Roifman ◽

D Hummel ◽

H Martinez-Valdez ◽

P Thorner ◽

P J Doherty ◽

...

Keyword(s):

T Cells ◽

Peripheral Blood ◽

Inbred Mice ◽

Pneumocystis Carinii ◽

Antigen Expression ◽

Class I ◽

Class I Mhc ◽

Cd8 Cells ◽

Mhc Antigen ◽

Selection Of

CD8 molecules expressed on the surface of a subset of T cells participate in the selection of class I MHC antigen-restricted T cells in the thymus, and in MHC-restricted immune responses of mature class I MHC antigen-restricted T cells. Here we describe an immune-deficient patient with lack of CD8+ peripheral blood cells. The patient presented with Pneumocystis carinii pneumonia and was unable to reject an allogeneic skin graft, but had normal primary and secondary antibody responses. Examination of the patient's thymus revealed that the loss of CD8+ cells occurred during intrathymic differentiation: the patient's immature cortical thymocytes included both CD4+ and CD8+ cells while the mature medullary cells expressed the CD4 but not the CD8 protein on their surface. Northern blot and polymerase chain reaction analyses revealed the presence of CD8 alpha and beta mRNA in the patient's thymus but not in the peripheral blood. Both class I MHC antigen expression and the expressed TCR V beta repertoire are normal in this patient. These data are consistent with an impaired selection of CD8+ cells in the patient's thymus and support the role of the CD8 surface protein in thymic selection previously characterized in genetically manipulated and inbred mice.

Download Full-text

Role of Class-II Major Histocompatibility Complex (MHC)-Antigen–Positive Donor Leukocytes in Transfusion-Induced Alloimmunization to Donor Class-I MHC Antigens

Blood ◽

10.1182/blood.v92.2.690 ◽

1998 ◽

Vol 92 (2) ◽

pp. 690-694 ◽

Cited By ~ 16

Author(s):

K.J. Kao ◽

M.L.U. del Rosario

Keyword(s):

Immune Response ◽

Peripheral Blood ◽

Class Ii ◽

Class I ◽

Mononuclear Leukocytes ◽

Class I Mhc ◽

Mhc Antigens ◽

Mhc Molecules ◽

Class Ii Mhc ◽

Mhc Antigen

Abstract It has been shown that peripheral-blood mononuclear leukocytes (MNL) are responsible for transfusion-induced alloimmunization to donor major histocompatability complex (MHC) antigens. However, it is not known which subset of MNL is responsible for this immune response. Because elimination of class-II MHC antigen-positive passenger leukocytes effectively prolongs the survival of allografts, it has been hypothesized that class-II positive MNL are responsible for immunizing transfusion recipients to donor MHC antigens. To test this hypothesis, two different approaches were used. First, we compared the alloantigenicity of BALB/c mice (H-2d) peripheral blood MNL before and after depletion of class-II positive cells. CBA mice (H-2k) were used as transfusion recipients. Antibody development to donor class-I H-2 antigens was determined by flow cytometry and enzyme-linked immunoassay. After four weekly transfusions of MNL depleted for class-II positive cells, only 25% of recipient mice developed antibodies to donor H-2d antigens. In contrast, all mice transfused with control MNL became immunized. Second, we studied the alloantigenicity of peripheral MNL from C57BL/6 mice (H-2b) with homozygous deficiency of class-II MHC molecules in H-2 disparate recipient mice. After transfusions with class-II MHC molecule-deficient MNL, 0% of BALB/c, 40% of C57BR, and 25% of CBA-recipient mice developed antibodies to donor H-2b antigen. All control recipient mice were immunized. The antibody activities of the controls were also higher than those in the treatment group who became immunized. Thus, our study shows that class-II MHC antigen-positive MNL play a significant role in transfusion-induced alloimmunization to donor class-I MHC antigens. The results also support the hypothesis that direct antigen presentation by donor class-II positive MNL to the immune system of transfusion recipients is critical for the initiation of humoral immune response to donor MHC antigens.

Download Full-text