Other search tools

About this data

The publication data currently available has been vetted by Vanderbilt faculty, staff, administrators and trainees. The data itself is retrieved directly from NCBI's PubMed and is automatically updated on a weekly basis to ensure accuracy and completeness.

If you have any questions or comments, please contact us.

Results: 1 to 3 of 3

Publication Record

Connections

Detection of rare antigen-presenting cells through T cell-intrinsic meandering motility, mediated by Myo1g.
Gérard A, Patino-Lopez G, Beemiller P, Nambiar R, Ben-Aissa K, Liu Y, Totah FJ, Tyska MJ, Shaw S, Krummel MF
(2014) Cell 158: 492-505
MeSH Terms: Animals, Antigen-Presenting Cells, Cell Membrane, Cell Movement, Immunologic Surveillance, Lymph Nodes, Mice, Minor Histocompatibility Antigens, Myosins, Receptors, Antigen, T-Cell, T-Lymphocytes
Show Abstract · Added January 21, 2015
To mount an immune response, T lymphocytes must successfully search for foreign material bound to the surface of antigen-presenting cells. How T cells optimize their chances of encountering and responding to these antigens is unknown. T cell motility in tissues resembles a random or Levy walk and is regulated in part by external factors including chemokines and lymph-node topology, but motility parameters such as speed and propensity to turn may also be cell intrinsic. Here we found that the unconventional myosin 1g (Myo1g) motor generates membrane tension, enforces cell-intrinsic meandering search, and enhances T-DC interactions during lymph-node surveillance. Increased turning and meandering motility, as opposed to ballistic motility, is enhanced by Myo1g. Myo1g acts as a "turning motor" and generates a form of cellular "flânerie." Modeling and antigen challenges show that these intrinsically programmed elements of motility search are critical for the detection of rare cognate antigen-presenting cells.
Copyright © 2014 Elsevier Inc. All rights reserved.
1 Communities
1 Members
0 Resources
11 MeSH Terms
Immune interactions in endometriosis.
Herington JL, Bruner-Tran KL, Lucas JA, Osteen KG
(2011) Expert Rev Clin Immunol 7: 611-26
MeSH Terms: Animals, Endometriosis, Environmental Exposure, Female, Humans, Immunologic Surveillance, Polychlorinated Dibenzodioxins, Progesterone, Teratogens
Show Abstract · Added May 29, 2014
Endometriosis is a common, complex gynecologic disorder characterized by the presence of endometrial glands and stroma at extrauterine (ectopic) sites. In women who develop this disease, alterations in specific biological processes involving both the endocrine and immune systems have been observed, which may explain the survival and growth of displaced endometrial tissue in affected women. In the past decade, a considerable amount of research has implicated a role for alterations in progesterone action at both eutopic and ectopic sites of endometrial growth which may contribute to the excessive inflammation associated with progression of endometriosis; however, it remains unclear whether these anomalies induce the condition or are simply a consequence of the disease process. In this article, we summarize current knowledge of alterations within the immune system of endometriosis patients and discuss how endometrial cells from women with this disease not only have the capacity to escape immunosurveillance, but also use inflammatory mechanisms to promote their growth within the peritoneal cavity. Finally, we discuss evidence that exposure to an environmental endocrine disruptor, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin, can mediate the development of an endometrial phenotype that exhibits both reduced progesterone responsiveness and hypersensitivity to proinflammatory stimuli mimicking the endometriosis phenotype. Future studies in women with endometriosis should consider whether a heightened inflammatory response within the peritoneal microenvironment contributes to the development and persistence of this disease.
0 Communities
3 Members
0 Resources
9 MeSH Terms
A highly immunogenic tumor transfected with a murine transforming growth factor type beta 1 cDNA escapes immune surveillance.
Torre-Amione G, Beauchamp RD, Koeppen H, Park BH, Schreiber H, Moses HL, Rowley DA
(1990) Proc Natl Acad Sci U S A 87: 1486-90
MeSH Terms: Animals, Cell Transformation, Neoplastic, Cells, Cultured, Clone Cells, Cytotoxicity, Immunologic, Exons, Female, Fibrosarcoma, Immunity, Cellular, Immunologic Surveillance, Lymphocyte Culture Test, Mixed, Mice, Mice, Inbred C3H, Mice, Nude, Neoplasms, Radiation-Induced, Plasmids, Restriction Mapping, Sarcoma, Experimental, Transfection, Transforming Growth Factors, Ultraviolet Rays
Show Abstract · Added May 3, 2013
A highly immunogenic C3H-derived UV-induced tumor was cotransfected with a murine transforming growth factor type beta 1 (TGF-beta 1) cDNA and a neomycin-resistance gene. Stable clones were isolated and used in vitro and in vivo to determine the effects of endogenously produced TGF-beta on cytolytic T-lymphocyte (CTL) responses. Tumor cells producing TGF-beta, though retaining expression for class I major histocompatibility complex molecules and the tumor-specific antigen, did not stimulate primary CTL responses in vitro and were not effective in vivo for directly stimulating primary CTL or in priming for CTL responses. Furthermore, TGF-beta-producing tumors grew progressively in transiently immunosuppressed mice without losing the tumor antigen; thus, TGF-beta produced by tumors may promote escape from immune surveillance.
0 Communities
1 Members
0 Resources
21 MeSH Terms