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Richard Bucala

Bio: Richard Bucala is an academic researcher from Yale University. The author has contributed to research in topics: Macrophage migration inhibitory factor & Cytokine. The author has an hindex of 119, co-authored 595 publications receiving 54607 citations. Previous affiliations of Richard Bucala include École Polytechnique Fédérale de Lausanne & Rockefeller University.


Papers
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Journal ArticleDOI
TL;DR: In this article, the authors investigated biological predictors for clinical outcomes in a dataset of 13,642 ambulatory and hospitalized adult COVID-19 patients, including younger (age < 65, n/= 566) and older (age ≥ 65,n/= 717) subjects, with in-depth analyses of inflammatory molecules, cytokines and comorbidities.

4 citations

Patent
14 Jan 2002
TL;DR: In this paper, a mouse model using the EL4 tumor, cultured splenocytes from tumor-primed mice secrete high levels of MIF following antigen stimulation in vitro.
Abstract: Regulation of expression of CTL activity by macrophage migration inhibitory factor (MIF) is disclosed. In a mouse model using the EL4 tumor, cultured splenocytes from tumor-primed mice secrete high levels of MIF following antigen stimulation in vitro. Parallel splenocytes treated with neutralizing anti-MIF mAb showed a significant increase in CTL response against tumor cells compared to control mAb-treated cultures, with elevated expression of IFN .gamma.. Histology of tumors from anti-MIF treated animals showed increases in infiltration of both CD4+ and CD8+ T cells, as well as apoptotic tumor cells, consistent with observed augmentation of CTL activity in vivo by anti-MIF, which was associated with enhanced expression of the common .gamma.c chain of the IL-2 receptor that mediates CD8+T cell survival. CD8+ cells of anti-MIF treated tumor-bearing mice showed increased migration into tumors of control mice. Methods for enhancing a CTL response by inhibition of MIF are disclosed.

4 citations

Journal ArticleDOI
TL;DR: The atypical cytokine MIF, but not its close homologue D-DT, promotes motility of cells that is independent of its main receptor CD74, suggesting a direct function of internalized MIF.
Abstract: Macrophage migration inhibitory factor (MIF) and its homologue D-dopachrome tautomerase (D-DT) are ubiquitous, pro-inflammatory cytokines with chemokine-like functions that coordinate a wide spectrum of biological activities like migration. Here, we biotin-tagged intracellular MIF/D-DT in vivo to identify important cytosolic interactors and found a plethora of actin cytoskeleton-associated proteins. While the CD74/CD44 receptor complex is essential for signalling transduction in fibroblasts by extracellular MIF/D-DT, our interactome data rather suggested direct effects. We thus investigated whether MIF/D-DT can modulate cell migration independent of CD74/CD44. To differentiate between receptor- and non-receptor-mediated motility, we treated fibroblasts that are deficient in CD74 and CD44 or that express both proteins with recombinant MIF/D-DT. Interestingly, only MIF could stimulate chemokinesis in the presence or absence of CD74/CD44. The pro-migratory effects of MIF depended on lipid raft/caveolae-mediated but not clathrin-mediated endocytosis, on its tautomerase activity and, likely, on its thiol protein oxidoreductase activity. As MIF treatment restrained actin polymerisation in vitro our findings establish a new intracellular role for MIF/D-DT in driving cell motility by modulating the actin cytoskeleton.

3 citations

Journal ArticleDOI
TL;DR: This study proves that haplotype frequencies and missing data probabilities are identifiable if and only if there is linkage disequilibrium between these markers under the general missing data model and extends the work to multi-allelic markers and observes a similar finding.
Abstract: It is common to have missing genotypes in practical genetic studies. The majority of the existing statistical methods, including those on haplotype analysis, assume that genotypes are missing at random—that is, at a given marker, different genotypes and different alleles are missing with the same probabilities. In our previous work, we demonstrated that the violation of this assumption may lead to serious bias in haplotype frequency estimates and haplotype association analysis. We proposed a general missing data model to simultaneously characterize missing data patterns across a set of two or more biallelic markers. We proved that haplotype frequencies and missing data probabilities are identifiable if and only if there is linkage disequilibrium between these markers under the general missing data model. In this study, we extend our work to multi-allelic markers and observe a similar finding. Simulation studies on the analysis of haplotypes consisting of two markers illustrate that our proposed model can ...

3 citations

Reference EntryDOI
TL;DR: An accurate identification and understanding of the various immunosuppressive factors that tumor cells employ to impair the host immune response is critical for the development of effective treatments for cancer patients.
Abstract: Tumor cells avoid attack from the host immune system by expressing a variety of different molecules including: cytokines, prostaglandins, polyamines, enzymes, cell surface receptors, and shed antigens. Cancers that are successful in evading host antitumor defenses tend to persist, enlarge, and ultimately metastasize. Thus, an accurate identification and understanding of the various immunosuppressive factors that tumor cells employ to impair the host immune response is critical for the development of effective treatments for cancer patients. Overcoming these evasive mechanisms may be the last major obstacle to the generation of universally successful cancer therapeutics. Keywords: Anergy; Indoleamine 2,3-dioxygenase; Polyamines; Tolerance; Tumor Infiltrating Lymphocyte

3 citations


Cited by
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08 Dec 2001-BMJ
TL;DR: There is, I think, something ethereal about i —the square root of minus one, which seems an odd beast at that time—an intruder hovering on the edge of reality.
Abstract: There is, I think, something ethereal about i —the square root of minus one. I remember first hearing about it at school. It seemed an odd beast at that time—an intruder hovering on the edge of reality. Usually familiarity dulls this sense of the bizarre, but in the case of i it was the reverse: over the years the sense of its surreal nature intensified. It seemed that it was impossible to write mathematics that described the real world in …

33,785 citations

Journal ArticleDOI
02 Apr 1999-Science
TL;DR: Adult stem cells isolated from marrow aspirates of volunteer donors could be induced to differentiate exclusively into the adipocytic, chondrocytic, or osteocytic lineages.
Abstract: Human mesenchymal stem cells are thought to be multipotent cells, which are present in adult marrow, that can replicate as undifferentiated cells and that have the potential to differentiate to lineages of mesenchymal tissues, including bone, cartilage, fat, tendon, muscle, and marrow stroma. Cells that have the characteristics of human mesenchymal stem cells were isolated from marrow aspirates of volunteer donors. These cells displayed a stable phenotype and remained as a monolayer in vitro. These adult stem cells could be induced to differentiate exclusively into the adipocytic, chondrocytic, or osteocytic lineages. Individual stem cells were identified that, when expanded to colonies, retained their multilineage potential.

20,479 citations

28 Jul 2005
TL;DR: PfPMP1)与感染红细胞、树突状组胞以及胎盘的单个或多个受体作用,在黏附及免疫逃避中起关键的作�ly.
Abstract: 抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1(PfPMP1)与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用,在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员,通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

18,940 citations