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Antigen

About: Antigen is a research topic. Over the lifetime, 170233 publications have been published within this topic receiving 6982342 citations. The topic is also known as: antibody generator & Antigen.


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Journal ArticleDOI
TL;DR: Experiments with both cytotoxic and inducer lymphocytes demonstrated that the T cells had to co-recognize antigen in association with one of these MHC-encoded molecules in order for activation to occur.
Abstract: One of the most important conceptual breakthroughs in cellular im­ munology during the 1970s was the realization that the influence of gene products of the major histocompatibility complex (MHC) on immune reactions stemmed largely from the central role they played in the activation of T lymphocytes (1 ). Experiments with both cytotoxic and inducer lymphocytes demonstrated that the T cells had to co-recognize antigen in association with one of these MHC-encoded molecules in order for activation to occur. Cytotoxic T cells required class I molecules whereas inducer T cells required class II molecules. Thus, in contrast to other cell-surface receptors specific for a single ligand (e.g. a hormone receptor) the antigen-specific receptor on T cells must form a ternary complex with two ligands. One of these ligands is a trans­ membrane glycoprotein on the surface of another cell; the other is often an unknown partial degradation product of the original antigen added to the cultures. As a consequence of this complexity, no simple ligand binding assays exist. All receptor interactions are measured with a biological assay, such as thymidine incorporation, which appears to reflect in a quantitative

866 citations

01 Jan 1994
TL;DR: The identification of another gene that also directs the expression of an antigen recognized on most melanomas by CTL clones that are restricted by HLA-A2 is reported, which is unrelated to any known gene.
Abstract: Summary It has been reported previously that antitumor cytolytic T lymphocyte (CTL) clones can be isolated from blood lymphocytes of HLA-A2 melanoma patients, after stimulation in vitro with autologous tumor cells, and that some of these CTL clones lyse most HLA-A2 melanomas. A first antigen recognized by such CTL clones was previously shown to be encoded by the tyrosinase gene. We report here the identification of another gene that also directs the expression of an antigen recognized on most melanomas by CTL clones that are restricted by HLA-A2. The gene, designated Melan-A, is unrelated to any known gene. It is 18 kb long and comprises five exons. Like the tyrosinase gene, it is expressed in most melanoma tumor samples and, among normal cells, only in melanocytes.

866 citations

Journal ArticleDOI
TL;DR: The special physiological relevance of this cytokine lies in the prevention and limitation of over-whelming specific and unspecific immune reactions and, in consequence, of tissue damage.

866 citations

Journal ArticleDOI
TL;DR: Dendritic cell responsiveness to type I interferon is required for the generation of antitumor T cell responses and tumor rejection.
Abstract: Cancer immunoediting is the process whereby the immune system suppresses neoplastic growth and shapes tumor immunogenicity. We previously reported that type I interferon (IFN-α/β) plays a central role in this process and that hematopoietic cells represent critical targets of type I IFN’s actions. However, the specific cells affected by IFN-α/β and the functional processes that type I IFN induces remain undefined. Herein, we show that type I IFN is required to initiate the antitumor response and that its actions are temporally distinct from IFN-γ during cancer immunoediting. Using mixed bone marrow chimeric mice, we demonstrate that type I IFN sensitivity selectively within the innate immune compartment is essential for tumor-specific T cell priming and tumor elimination. We further show that mice lacking IFNAR1 (IFN-α/β receptor 1) in dendritic cells (DCs; Itgax-Cre+Ifnar1f/f mice) cannot reject highly immunogenic tumor cells and that CD8α+ DCs from these mice display defects in antigen cross-presentation to CD8+ T cells. In contrast, mice depleted of NK cells or mice that lack IFNAR1 in granulocytes and macrophage populations reject these tumors normally. Thus, DCs and specifically CD8α+ DCs are functionally relevant targets of endogenous type I IFN during lymphocyte-mediated tumor rejection.

866 citations

Journal Article
TL;DR: Enzymatic digestion experiments showed that this antigen is highly susceptible to protease treatment, and the antigen cannot be extracted by 0.1 normal HCl, indicating that Ki-67 antigen is a nonhistone protein.
Abstract: The monoclonal antibody Ki-67 detects a human nuclear antigen that is present in proliferating cells, but absent in quiescent cells. The aim of this study was to characterize the Ki-67 antigen by means of immunobiochemical and molecular biology techniques. Enzymatic digestion experiments showed that this antigen is highly susceptible to protease treatment, and the antigen cannot be extracted by 0.1 normal HCl, indicating that Ki-67 antigen is a nonhistone protein. Immunoblot analysis of cell lysates with Ki-67 showed a double band with apparent molecular weights of 395 kd and 345 kd, regardless of whether the gels were run under reducing or nonreducing conditions. It is noteworthy that these bands were exclusively detectable in lysates prepared from proliferating cells, whereas they were absent in lysates obtained from quiescent cells. These immunobiochemical data are further substantiated by our molecular cloning approaches. By means of immunocloning with Ki-67, the authors isolated and sequenced several cDNA fragments from lambda gt11 libraries. A 1095-bp fragment gave a strong hybridization signal at 7.5 to 9.5 kb in Northern blot analysis with RNA prepared from proliferating cells, whereas it was negative with RNA prepared from quiescent cells. This cDNA fragment could be bacterially expressed, and in subsequent immunoblot analysis Ki-67 reacted exclusively with those fusion proteins that were derived from bacteria containing the insert in the right reading frame.

865 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20244
20233,983
20225,279
20213,228
20203,444
20193,267