Class I Antigen Expression in Line 1 Cells: Molecular Biology and Immunological Effects

H-2 Antigens ◽  
1987 ◽  
pp. 611-622
Author(s):  
John G. Frelinger ◽  
Karen M. Cerosaletti ◽  
David W. Bahler ◽  
Lee W. Harwell ◽  
Edith M. Lord
Keyword(s):  
Molecular Biology ◽  
Antigen Expression ◽  
Class I ◽  
Immunological Effects

Immunohistological evaluation of MHC class I and II antigen expression on nevi and melanoma: relation to biology of melanoma

Pathology ◽  
1987 ◽  
Vol 19 (4) ◽  
pp. 339-346 ◽  
Author(s):  
Gennaro D’Alessandro ◽  
Peter Hersey ◽  
Ibrahim Zardawi ◽  
Julienne Grace ◽  
William H. McCarthy
Keyword(s):  
Mhc Class I ◽  
Antigen Expression ◽  
Class I

H-2 class I antigen expression on mouse teratocarcinoma cell lines

1985 ◽  
Vol 22 (6) ◽  
pp. 543-552 ◽  
Author(s):  
P. D�mant ◽  
M. Oudshoorn-Snoek
Keyword(s):  
Cell Lines ◽  
Antigen Expression ◽  
Class I ◽  
Teratocarcinoma Cell ◽  
Mouse Teratocarcinoma

scholarly journals Variation of class I HLA antigen expression among platelet density cohorts: a possible index of platelet age?

Blood ◽  
1988 ◽  
Vol 71 (2) ◽  
pp. 516-519
Author(s):  
J Pereira ◽  
C Cretney ◽  
RH Aster
Keyword(s):  
Hla Antigens ◽  
Antigen Expression ◽  
High Density ◽  
Class I ◽  
Surface Markers ◽  
Low Density ◽  
Hla Antigen ◽  
The Difference ◽  
Hla Molecules

Platelet alloantigens and other surface markers were studied in platelet cohorts of different mean density, using monoclonal and polyclonal probes. High density (HD) platelets expressed 12% more P1A1 molecules (46,942) than low density (LD) platelets (41,892). However, LD platelets carried 42% more HLA-A2 molecules (6,267 +/- 184) than HD platelets (4,406 +/- 232) (P less than .01) and 55% more class I HLA antigens (17,034 +/- 2,062 v 11,007 +/- 2,190) (P = .05). The platelet subpopulations did not differ in their content of glycoprotein (GP)IIb/IIIa complex or Baka antigen. The difference in expression of class I HLA antigens on HD and LD platelets is consistent with two possibilities: either class I HLA molecules are acquired from plasma or they are released into plasma as platelets age in circulation. Accordingly, class I HLA molecules may provide a useful marker of platelet age.

scholarly journals Widespread and selective induction of major histocompatibility complex-determined antigens in vivo by gamma interferon.

1985 ◽  
Vol 162 (5) ◽  
pp. 1645-1664 ◽  
Author(s):  
M J Skoskiewicz ◽  
R B Colvin ◽  
E E Schneeberger ◽  
P S Russell
Keyword(s):  
Dendritic Cells ◽  
Small Intestine ◽  
Antigen Expression ◽  
Class Ii ◽  
Gamma Interferon ◽  
The Body ◽  
Class I ◽  
Ifn Gamma ◽  
Histocompatibility Complex

gamma Interferon (IFN-gamma) caused remarkable increases in class I (H-2Kk) and class II (I-Ak) antigens throughout the body by 6-9 d. Heart, kidney, and adrenals showed increases of 4-8 times their previous levels of class I antigen content, while the pancreas and small intestine increased 13-17-fold. Lesser increases were found in spleen, liver, and lung, which showed higher resting antigenic potency. Increases of class II antigenicity of 6-10-fold were found in heart, kidney, pancreas, lung, liver, adrenal, and small intestine, with lesser increases in thymus and spleen, and none in lymph node. Topographical analysis revealed that IFN-gamma induced class I and II antigens on most tissues in a highly selective fashion. For example, the renal proximal tubules expressed large amounts of both class I and II antigens, whereas the distal tubules and collecting ducts did not. In some epithelial cells class I and II determinants were induced only on the basal aspects of the cell membrane. IFN-gamma caused a remarkable increase in class II-positive dendritic cells in the liver, pancreas, salivary glands, and thyroid. Whether these cells were of local or systemic origin is uncertain, but the finding of a simultaneous depletion of dendritic cells from lymph nodes and spleen raises the possibility that they may have been derived, at least in part, from these sites. The dynamic and selective induction of class I and II antigen expression by IFN-gamma is likely to be important in regulation of the immune response in tissues.

scholarly journals Stability of antigens on leukocytes in banked platelet concentrates: decline in HLA-DR antigen expression and mixed lymphocyte culture stimulating capacity following storage

Blood ◽  
1988 ◽  
Vol 72 (3) ◽  
pp. 867-872
Author(s):  
ME Sherman ◽  
WH Dzik
Keyword(s):  
Hla Antigens ◽  
Human Leukocyte ◽  
Antigen Expression ◽  
Class Ii ◽  
Mixed Lymphocyte Culture ◽  
Lymphocyte Culture ◽  
Class I ◽  
Platelet Concentrates ◽  
Platelet Storage ◽  
Leukocyte Antigens

Abstract Repeatedly transfused thrombocytopenic patients frequently form antibodies directed against human leukocyte antigens (HLA) and become unresponsive to random donor platelet transfusions. Although exposure to foreign antigens borne on donor leukocytes appears necessary to provoke primary sensitization, the stability of leukocyte antigens during routine platelet storage is largely unknown. Accordingly, we serially measured the expression of surface markers on leukocytes derived from platelet concentrates during storage using immunofluorescence and flow cytometry. Our results indicate that the expression of class I HLA antigens, Leu-4 (T cell), and HLe-1 (pan leukocyte) remained stable on lymphocytes under standard platelet storage conditions, but that the percentage of lymphocytes bearing class II HLA antigens declined significantly over time. This decline in lymphocyte HLA class II expression was associated with a significantly diminished ability of stored leukocytes to stimulate blastogenesis in mixed lymphocyte culture. However, leukocytes retained the ability to respond in mixed lymphocyte culture (MLC) following storage. We also performed studies on lymphocytes cultured in the presence of cyclohexamide, which suggested that the expression of class I HLA antigens and B2 microglobulin are highly sensitive to the inhibition of protein synthesis, whereas the expression of class II HLA antigens, Leu- 4, and HLe-1 are not. Our results may prove useful in understanding the mechanisms that lead to platelet refractoriness and in designing strategies to prevent HLA alloimmunization.

scholarly journals Abnormalities in HLA Class I Antigen Expression by Melanoma Cells: Structural Characterization and Functional Implications

1993 ◽  
Vol 100 (2) ◽  
pp. S226-S230 ◽  
Author(s):  
Sebastiano Gattoni-Celli ◽  
Lidio Calorini ◽  
Hugh Randolph Byers ◽  
Takafumi Etoh ◽  
Zhigang Wang ◽  
...  
Keyword(s):  
Structural Characterization ◽  
Hla Class I ◽  
Antigen Expression ◽  
Melanoma Cells ◽  
Class I ◽  
Hla Class I Antigen ◽  
Functional Implications

scholarly journals Kirsten murine sarcoma virus abolishes interferon gamma-induced class II but not class I major histocompatibility antigen expression in a murine fibroblast line.

1988 ◽  
Vol 167 (2) ◽  
pp. 706-711 ◽  
Author(s):  
D J Maudsley ◽  
A G Morris
Keyword(s):  
Leukemia Virus ◽  
Constitutive Expression ◽  
Antigen Expression ◽  
Class Ii ◽  
Class I ◽  
Ras Gene ◽  
Ifn Gamma ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Murine Sarcoma

The effect of infecting fibroblasts with Kirsten murine sarcoma virus/murine leukemia virus (Ki-MSV/MLV) on constitutive and IFN-gamma-induced H-2 antigen expression was investigated. The fibroblasts used were two established cell lines (C3H10T1/2 and BALB/c3T3) and fresh embryo fibroblasts from C3H mice. Class I antigens were expressed constitutively by BALB/c3T3; infection with MLV, MSV or the two together had little effect on this constitutive expression. Class I antigens (H-2K, H-2D) were strongly induced on all three types of fibroblast by rIFN-gamma, and infection had little effect on this. None of the fibroblasts expressed constitutively detectable levels of class II antigen; however, C3H10T1/2 fibroblasts could be induced for both H-2A and H-2E by IFN-gamma. Infection of C3H10T1/2 with helper-free Ki-MSV, or MSV together with MLV, completely abolished this induction of class II antigens, while infection with MLV alone had little effect, implying that the abolition of class II induction was due to genomic regions of Ki-MSV not shared with Ki-MLV, probably the v-Ki-ras gene.

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