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Jan Klein

Bio: Jan Klein is an academic researcher from Max Planck Society. The author has contributed to research in topics: Major histocompatibility complex & Antigen. The author has an hindex of 74, co-authored 423 publications receiving 23904 citations. Previous affiliations of Jan Klein include Cleveland Clinic & National Institute of Genetics.


Papers
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Book
01 Jan 1986
TL;DR: The Story TheGene: Organismic approach The Gene: Molecular approach The Protein The Antibody The Cell Function The Population Sociology Evolution Index.
Abstract: The Story The Gene: Organismic Approach The Gene: Molecular Approach The Protein The Antibody The Cell Function The Population Sociology Evolution Index.

1,284 citations

BookDOI
01 Jan 1975

1,051 citations

Journal ArticleDOI
TL;DR: A man dies because his body has rejected a heart transplant; a woman is crippled by rheumatoid arthritis; a child goes into a coma that is brought on by cerebral malaria; another child dies of an infection because of an immunodeficiency; an elderly man has advanced hepatic cirrhosis caused by iron overload.
Abstract: A man dies because his body has rejected a heart transplant; a woman is crippled by rheumatoid arthritis; a child goes into a coma that is brought on by cerebral malaria; another child dies of an infection because of an immunodeficiency; an elderly man has advanced hepatic cirrhosis caused by iron overload. These five clinical situations are as diverse as can be, yet all have one thing in common: the cause of all of them involves the human leukocyte antigen (HLA) system, the human version of the major histocompatibility complex (MHC). Malfunction of the HLA system, which is at the . . .

838 citations

Journal ArticleDOI
TL;DR: Adult thymectomized, irradiated and bone marrow reconstituted mice, transplanted with an irradiated thymus of A origin, generate virus-specific cytotoxic T cells specific for infected A targets but not for B targets; this result formally demonstrates the crucial role of thymic epithelial cells in the differentiation of anti-self-H-2 specificities of T cells.
Abstract: In the thymus, precursor T cells differentiate recognition structures for self that are specific for the H-2K, D, and I markers expressed by the thymic epithelium. Thus recognition of self-H-2 differentiates independently of the T cells H-2 type and independently of recognition of nonself antigen X. This is readily compatible with dual recognition by T cells but does not formally exclude a single recognition model. These conclusions derive from experiments with bone marrow and thymic chimeras. Irradiated mice reconstituted with bone marrow to form chimeras of (A X B)F1 leads to A type generate virus-specific cytotoxic T cells for infected targets A only. Therefore, the H-2 type of the host determines the H-2-restricted activity of killer T cells alone. In contrast, chimeras made by reconstituting irradiated A mice with adult spleen cells of (A X B)F1 origin generate virus-specific cytotoxic activity for infected A and B targets, suggesting that mature T cells do not change their self-specificity readily. (A X B)F1 leads to (A X C)F1 and (KAIA/DC) leads to (KAIA/DB) irradiation bone marrow chimeras responded against infected A but not B or C targets. This suggests that cytotoxicity is not generated against DC because it is abscent from the host's thymus epithelium and not against DB because it is not expressed by the reconstituting lymphoreticular system. (KBIB/DA) leads to (KCIC/DA) K, I incompatible, or completely H-2 incompatible A leads to B chimeras fail to generate any measurable virus specific cytotoxicity, indicating the necessity for I-specific helper T cells for the generation of killer T cells. Finally adult thymectomized, irradiated and bone marrow reconstituted (A X B)F1 mice, transplanted with an irradiated thymus of A origin, generate virus-specific cytotoxic T cells specific for infected A targets but not for B targets; this result formally demonstrates the crucial role of thymic epithelial cells in the differentiation of anti-self-H-2 specificities of T cells.

833 citations

Journal ArticleDOI
TL;DR: The major histocompatibility complex (MHC) has been given different names in different species (Klein 1986) and if the trend in choosing common names for MHC symbols were to continue, chaos would soon ensue because the authors can expect MHCs in many different species to be identified in the future.
Abstract: The major histocompatibility complex (MHC) has been given different names in different species (Klein 1986). It is designatedH-2 in the mouse, HLA in humans, B in the domestic fowl, RT1 in the rat, and Smh in the mole rat. In most other species that have been studied, the MHC is referred to by the LA symbol (for lymphocyte or leukocyte antigen), prefixed by an abbreviation of the species’ common name. Thus, it is called ChLa in the chimpanzee, GoLA in the gorilla, RhLA in the rhesus macaque, RLA in the rabbit, BoLA in the domestic cattle, SLA in the pig, and so on. This practice has two problems associated with it. First, MHC products are expressed on many other tissues in addition to lymphocyte or leukocyte (and lymphocytes express many other antigens in addition to those controlled by the MHC) and their antigenicity is secondary to their biological function. Second, the use of common names to identify a species is a potential source of confusion. Common names are notoriously vague and imprecise. The designation “lemur”, for example, can refer to any of the genera Lemur, Hapalemur, Varecia, Lepilemur; Avahi, Propithecus, and Indri, of which only the first four belong to the family Lemuridae; the last three are members of the family Indriidae. A “bushbaby” can be a Galago, Otolemur, or Euoticus. A “mouse” could be a Notomys, ylcomys, Uranomys, Pogomys, Chiruromys, Chiropodomys, Neohydromys, and so on. Obviously, common names not only fail to identify the species appropriately, they often do not even identify the genes or the family. If the trend in choosing common names for MHC symbols were to continue, chaos would soon ensue because we can expect MHCs in many different species to be identified in the future.

539 citations


Cited by
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Journal ArticleDOI
Eric S. Lander1, Lauren Linton1, Bruce W. Birren1, Chad Nusbaum1  +245 moreInstitutions (29)
15 Feb 2001-Nature
TL;DR: The results of an international collaboration to produce and make freely available a draft sequence of the human genome are reported and an initial analysis is presented, describing some of the insights that can be gleaned from the sequence.
Abstract: The human genome holds an extraordinary trove of information about human development, physiology, medicine and evolution. Here we report the results of an international collaboration to produce and make freely available a draft sequence of the human genome. We also present an initial analysis of the data, describing some of the insights that can be gleaned from the sequence.

22,269 citations

Journal Article
TL;DR: For the next few weeks the course is going to be exploring a field that’s actually older than classical population genetics, although the approach it’ll be taking to it involves the use of population genetic machinery.
Abstract: So far in this course we have dealt entirely with the evolution of characters that are controlled by simple Mendelian inheritance at a single locus. There are notes on the course website about gametic disequilibrium and how allele frequencies change at two loci simultaneously, but we didn’t discuss them. In every example we’ve considered we’ve imagined that we could understand something about evolution by examining the evolution of a single gene. That’s the domain of classical population genetics. For the next few weeks we’re going to be exploring a field that’s actually older than classical population genetics, although the approach we’ll be taking to it involves the use of population genetic machinery. If you know a little about the history of evolutionary biology, you may know that after the rediscovery of Mendel’s work in 1900 there was a heated debate between the “biometricians” (e.g., Galton and Pearson) and the “Mendelians” (e.g., de Vries, Correns, Bateson, and Morgan). Biometricians asserted that the really important variation in evolution didn’t follow Mendelian rules. Height, weight, skin color, and similar traits seemed to

9,847 citations

Journal ArticleDOI
TL;DR: The Bayesian Evolutionary Analysis by Sampling Trees (BEAST) software package version 1.7 is presented, which implements a family of Markov chain Monte Carlo algorithms for Bayesian phylogenetic inference, divergence time dating, coalescent analysis, phylogeography and related molecular evolutionary analyses.
Abstract: Computational evolutionary biology, statistical phylogenetics and coalescent-based population genetics are becoming increasingly central to the analysis and understanding of molecular sequence data. We present the Bayesian Evolutionary Analysis by Sampling Trees (BEAST) software package version 1.7, which implements a family of Markov chain Monte Carlo (MCMC) algorithms for Bayesian phylogenetic inference, divergence time dating, coalescent analysis, phylogeography and related molecular evolutionary analyses. This package includes an enhanced graphical user interface program called Bayesian Evolutionary Analysis Utility (BEAUti) that enables access to advanced models for molecular sequence and phenotypic trait evolution that were previously available to developers only. The package also provides new tools for visualizing and summarizing multispecies coalescent and phylogeographic analyses. BEAUti and BEAST 1.7 are open source under the GNU lesser general public license and available at http://beast-mcmc.googlecode.com and http://beast.bio.ed.ac.uk

9,055 citations

01 Sep 2012
TL;DR: In this article, a Mars Exploration Program lesson was prepared by Arizona State University's Mars Education Program, under contract to NASA's Jet Propulsion Laboratory, a division of the California Institute of Technology.
Abstract: 1 On behalf of NASA’s Mars Exploration Program, this lesson was prepared by Arizona State University’s Mars Education Program, under contract to NASA’s Jet Propulsion Laboratory, a division of the California Institute of Technology. These materials may be distributed freely for non-commercial purposes. Copyright 2014; 2012; 2010; 2000. Last edited: April 24, 2014 Marsbound! Mission to the Red Planet

4,486 citations