scholarly journals Cell immunity at pregnant women with autoimmune thyroiditis and gestosis

2002 ◽  
Vol 1 (1) ◽  
pp. 57-62
Author(s):  
A. Sh. Makhmuthodzhayev ◽  
L. M. Ogorodova ◽  
I. D. Evtushenko ◽  
A. V. Holopov ◽  
E. L. Timoshina ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Pregnant Women ◽  
Mhc Class Ii ◽  
Autoimmune Thyroiditis ◽  
Lymphocyte Subsets ◽  
Histocompatibility Complex ◽  
Cell Immunity ◽  
Hla Dr ◽  
Activated T Lymphocytes ◽  
A Prospective Study

In a prospective study the group of 60 women with AIT and thyroidological uneventful control women, matched for age and parity (n = 30) were tested at 12 and 32 weeks gestation for percentages of peripheral blood lymphocyte subsets (CD3, CD4, CD8, CD16, HLA-DR major histocompatibility complex (MHC)-class II), IL-2, IFN-gamma, TPO-Abs, TSH and thyroxin. Twenty five pregnant women with AIT (41,7%) developed preeclampsia (against 16,7% in control). Pregnancyrelated CMI alterations consisted of low percentages of CD16+ NK cells and all subpopulations of T-cells at 12 weeks gestation. The development of preeclampsia in women with AIT was accompanied with increasing percentage of HLADR+ T- lymphocytes. The high levels of TPO-Abs and activated T-lymphocytes in pregnant women with autoimmune thyroiditis has been suggested as a predictor for later preeclampsia development.

scholarly journals Major histocompatibility complex class II+B7-1+ tumor cells are potent vaccines for stimulating tumor rejection in tumor-bearing mice.

1995 ◽  
Vol 181 (2) ◽  
pp. 619-629 ◽  
Author(s):  
S Baskar ◽  
L Glimcher ◽  
N Nabavi ◽  
R T Jones ◽  
S Ostrand-Rosenberg
Keyword(s):  
Major Histocompatibility Complex ◽  
Tumor Cells ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Genetically Engineered ◽  
Tumor Rejection ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Cell Immunity ◽  
Sarcoma Cells

Mice carrying large established major histocompatibility complex (MHC) class 1+ sarcoma tumors can be successfully treated by immunization with genetically engineered sarcoma cells transfected with syngeneic MHC class II plus B7-1 genes. This approach is significantly more effective than previously described strategies using cytokine- or B7-transduced tumor cells which are only effective against smaller tumor loads, and which cannot mediate regression of longer-term established tumors. The most efficient tumor rejection occurs if both the class II and B7-1 molecules are coexpressed on the same tumor cell. Immunity induced by immunization with class II+B7-1(+)-transfected sarcoma cells involves CD4+ and CD8+ T cells, suggesting that the increased effectiveness of the transfectants is due to their ability to activate both of these T cell populations.

scholarly journals Expansion of activated T lymphocytes (CD3+HLA/DR+) detectable in early stages of HIV-1 infection

1990 ◽  
Vol 68 (8) ◽  
pp. 393-396 ◽  
Author(s):  
J. R. Bogner ◽  
A. Matuschke ◽  
B. Heinrich ◽  
M. A. Schreiber ◽  
C. Nerl ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Early Stages ◽  
Hla Dr ◽  
Activated T Lymphocytes ◽  
Hiv 1

scholarly journals Specificity of Effector T Lymphocytes in Autologous Graft-Versus-Host Disease: Role of the Major Histocompatibility Complex Class II Invariant Chain Peptide

Blood ◽  
1997 ◽  
Vol 89 (6) ◽  
pp. 2203-2209 ◽  
Author(s):  
Allan D. Hess ◽  
Emilie C. Bright ◽  
Christopher Thoburn ◽  
Georgia B. Vogelsang ◽  
Richard J. Jones ◽  
...  
Keyword(s):  
T Cells ◽  
Major Histocompatibility Complex ◽  
T Lymphocytes ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Effector T Cells ◽  
Invariant Chain ◽  
Target Cells ◽  
Graft Versus Host ◽  
Histocompatibility Complex

Abstract Administration of the immunosuppressive drug cyclosporine after autologous bone marrow transplantation induces a systemic autoimmune syndrome resembling graft-versus-host disease (GVHD). This syndrome termed autologous GVHD has significant antitumor activity. Associated with autologous GVHD is the development of T lymphocytes that recognize major histocompatibility complex (MHC) class II determinants, including self. The present studies attempted to characterize and define the molecular specificity of the effector T lymphocytes in autologous GVHD induced in patients with metastatic breast cancer. The results suggest that the effector cells associated with human autologous GVHD are CD8+ T lymphocytes expressing the α/β T-cell receptor. Additional studies show that the effector T cells recognize MHC class II antigens in association with a peptide from the invariant chain (CLIP). Pretreatment of autologous lymphoblast target cells with anti-CLIP antibody completely blocked lysis mediated by autologous GVHD effector T cells. On the other hand, force loading this peptide markedly enhanced the susceptibility of the target cells to recognition by the autoreactive T cells. The recognition of the MHC class II CLIP complex may account for the novel specificity of the effector T cells associated with human autologous GVHD. Moreover, identification of the target peptide may allow for the development of novel immunotherapeutic strategies to enhance the antitumor efficacy of autologous GVHD.

scholarly journals HLA-DM Interactions with Intermediates in HLA-DR Maturation and a Role for HLA-DM in Stabilizing Empty HLA-DR Molecules

1996 ◽  
Vol 184 (6) ◽  
pp. 2153-2166 ◽  
Author(s):  
Lisa K. Denzin ◽  
Craig Hammond ◽  
Peter Cresswell
Keyword(s):  
Mhc Class Ii ◽  
Antigen Processing ◽  
Class Ii ◽  
Physical Interaction ◽  
Antigenic Peptides ◽  
Histocompatibility Complex ◽  
Chain Complexes ◽  
Hla Dr

Major histocompatibility complex (MHC) class II–positive cell lines which lack HLA-DM expression accumulate class II molecules associated with residual invariant (I) chain fragments (class II–associated invariant chain peptides [CLIP]). In vitro, HLA-DM catalyzes CLIP dissociation from class II–CLIP complexes, promoting binding of antigenic peptides. Here the physical interaction of HLA-DM with HLA-DR molecules was investigated. HLA-DM complexes with class II molecules were detectable transiently in cells, peaking at the time when the class II molecules entered the MHC class II compartment. HLA-DR αβ dimers newly released from I chain, and those associated with I chain fragments, were found to associate with HLA-DM in vivo. Mature, peptide-loaded DR molecules also associated at a low level. These same species, but not DR-I chain complexes, were also shown to bind to purified HLA-DM molecules in vitro. HLA-DM interaction was quantitatively superior with DR molecules isolated in association with CLIP. DM-DR complexes generated by incubating HLA-DM with purified DR αβCLIP contained virtually no associated CLIP, suggesting that this superior interaction reflects a prolonged HLA-DM association with empty class II dimers after CLIP dissociation. Incubation of peptide-free αβ dimers in the presence of HLA-DM was found to prolong their ability to bind subsequently added antigenic peptides. Stabilization of empty class II molecules may be an important property of HLA-DM in facilitating antigen processing.

Clinical utility of serologic HLA-DR antigen identification using activated T lymphocytes

1986 ◽  
Vol 16 (3) ◽  
pp. 295-303 ◽  
Author(s):  
Patrick W. Adams ◽  
Ronald M. Ferguson ◽  
Smita Vaidya ◽  
Charles G. Orosz
Keyword(s):  
T Lymphocytes ◽  
Clinical Utility ◽  
Hla Dr ◽  
Activated T Lymphocytes

scholarly journals HLA-DRB1 polymorphism determines susceptibility to autoimmune thyroiditis in transgenic mice: definitive association with HLA-DRB1*0301 (DR3) gene.

1996 ◽  
Vol 184 (3) ◽  
pp. 1167-1172 ◽  
Author(s):  
Y C Kong ◽  
L C Lomo ◽  
R W Motte ◽  
A A Giraldo ◽  
J Baisch ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Mhc Class Ii ◽  
Autoimmune Thyroiditis ◽  
Class Ii ◽  
Experimental Autoimmune Thyroiditis ◽  
Autoimmune Thyroid Diseases ◽  
Human Major Histocompatibility Complex ◽  
Autoimmune Thyroid ◽  
Histocompatibility Complex ◽  
Hla Dr3

Familial clustering of autoimmune thyroid diseases has led to studies of their association with human major histocompatibility complex (MHC) class II genes. One such gene implicated in Hashimoto's thyroiditis (HT) is HLA-DR3, but the association is weak and is contradicted by other reports. On the other hand, murine experimental autoimmune thyroiditis (EAT), a model for HT, presents a clear linkage with MHC class II. Moreover, it is inducible with thyroglobulin (Tg), the common autoantigen in either species. Immunization of HLA-DRB1* 0301 (DR3) transgenic mice with mouse or human Tg resulted in severe thyroiditis. In contrast, transgenic mice expressing the HLA-DRB1*1502 (DR2) gene were resistant to EAT. Our studies show that HLA-DRB1 polymorphism determines susceptibility to autoimmune thyroiditis and implicate Tg as an important autoantigen.

scholarly journals HLA-DR alleles differ in their ability to present staphylococcal enterotoxins to T cells.

1990 ◽  
Vol 172 (3) ◽  
pp. 709-717 ◽  
Author(s):  
A Herman ◽  
G Croteau ◽  
R P Sekaly ◽  
J Kappler ◽  
P Marrack
Keyword(s):  
T Cells ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Human Class ◽  
Staphylococcal Enterotoxins ◽  
Histocompatibility Complex ◽  
Hla Dr ◽  
Specific Manner ◽  
Class Ii Antigens ◽  
Mhc Class Ii Molecules

Staphylococcal enterotoxins (SEs) have been shown to bind to major histocompatibility complex (MHC) class II proteins and stimulate T cells in a V beta-specific manner, and these V beta specificities for various SEs have been well documented in mice and humans. This study was undertaken in order to examine the ability of human class II molecules to present SEs to human and murine T cell hybridomas. Using a panel of transfectants expressing individual HLA class II antigens, we have shown that HLA-DR alleles differ in their ability to bind and present SEs. Since the HLA-DR proteins share a common alpha chain, these results indicate that the polymorphic beta chain plays an important role in SE binding and presentation to T cells. In addition, we have shown that human class II isotypes markedly differ in their ability to present SEs. The results of this study should provide information on the region of MHC class II molecules that interacts with foreign, and perhaps self, super-antigens.

scholarly journals Two DNA-binding proteins discriminate between the promoters of different members of the major histocompatibility complex class II multigene family

1990 ◽  
Vol 10 (3) ◽  
pp. 965-971
Author(s):  
M Kobr ◽  
W Reith ◽  
C Herrero-Sanchez ◽  
B Mach
Keyword(s):  
Gene Expression ◽  
Major Histocompatibility Complex ◽  
Mhc Class Ii ◽  
Dna Sequences ◽  
Multigene Family ◽  
Class Ii ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Hla Dr ◽  
Beta Chain Genes

The regulation of major histocompatibility complex (MHC) class II gene expression is a key feature of the control of normal and abnormal immune responses. In humans, class II alpha - and beta-chain genes are organized in a multigene family with three distinct subregions, HLA-DR, -DQ, and -DP. The regulation of these genes is generally coordinated, and their promoters contain highly conserved motifs, in particular the X and Y boxes. We have identified five distinct proteins that bind to specific DNA sequences within the first 145 base pairs of the HLA-DR promoter, a segment known to be functionally essential for class II gene regulation. Among these, RF-X is of special interest, since mutants affected in the regulation of MHC class II gene expression have a specific defect in RF-X binding. Unexpectedly, RF-X displays a characteristic gradient of binding affinities for the X boxes of three alpha-chain genes (DRA greater than DPA much greater than DQA). The same observation was made with recombinant RF-X. We also describe a novel factor, NF-S, which bound to the spacer region between the X and Y boxes of class II promoters. NF-S exhibited a reverse gradient of affinity compared with RF-X (DQA greater than DPA much greater than DRA). As expected, RF-X bound well to the mouse IE alpha promoter, while NF-S bound well to IA alpha. The drastic differences in the binding of RF-X and NF-S to different MHC class II promoters contrasts with the coordinate regulation of HLA-DR, -DQ, and -DP genes.

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