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At least 469 records · Page 26Linked to original sources
PubMed2000

Chemokines in tissue-specific and microenvironment-specific lymphocyte homing.

This review describes recent breakthroughs in our understanding of the roles played by chemokines in lymphocyte trafficking. These include the first demonstration that chemokines control lymphocyte/vascular recognition by shear-resistant rapid adhesion; the first example of specialized tissue-specific homing mediated by chemokines; and the implication that chemokines may control microenvironmental segregation within lymphoid organs.

Cell Adhesion↗
PubMed2003

B cells as effectors.

B cells act as immune effectors, primarily through antigen-specific clonal expansion and plasma-cell differentiation. B1 (CD5(+)) B cells and marginal zone B cells dominate T-cell independent humoral responses under the molecular control of activated dendritic cells. Helper T cell-regulated B-cell responses draw on follicular B cells as precursors and rely on qualitatively different patterns of immune synapse formation to regulate B-cell fate. These activities culminate in the germinal center reaction, during which somatic hypermutation and antigen-driven selection produce and preserve high-affinity plasma cells with extended longevity and memory B cells as the sensitized precursors for antigen recall.

Animals↗
PubMed1997

Viruses use stealth technology to escape from the host immune system.

In this review, we focus on recent investigations that reveal novel mechanisms by which viruses evade detection and elimination by the host immune system. In particular, we consider the evasion mechanisms of five persistent viruses: herpes simplex virus, human cytomegalovirus, mouse cytomegalovirus, Epstein-Barr virus and adenovirus. Unravelling the strategies used by viruses to survive within the host could identify new targets for antiviral drugs and for improved vaccines. Identification of the mechanisms that underlie these strategies might also reveal new, fundamental features of biology that occur in uninfected cells and are exploited by viruses.

Adenoviridae↗
PubMed2002

About CD4pos CD25pos regulatory cells.

Autoreactive cells that escape from thymic negative selection are either anergized or counter-regulated in the peripheral lymphoid organs by regulatory T (Treg) cells. Most investigated Treg cells are CD4pos cells expressing the alpha chain of the IL-2 receptor (CD25). Absence of this particular population leads to the development of a wide range of autoimmune disorders, suggesting a critical role for CD4pos CD25pos cells in the maintenance of normal immune homeostasis. Numerous studies have aimed at unraveling the mechanisms of regulation, focusing mainly on naturally occurring Treg cells (generated in naive animals) and regulation of CD4pos autoreactive cells. In contrast, generation following antigenic priming of CD4pos CD25pos Treg cells with non-self (viral) antigen specificity and regulation of virus-activated CD4pos and CD8pos cells remain to be investigated. In this review, we describe the data collected over the past few years of intense focus on CD4pos CD25pos Treg cells and present our approach to investigate the generation of antigen-specific Treg cells during the course of an anti-viral immune response.

Animals↗
PubMed2000

Is Crohn's disease an immunodeficiency? A hypothesis suggesting possible early events in the pathogenesis of Crohn's disease.

The current hypothesis for the etiology of Crohn's disease proposes an excessive immune response, largely T-cell driven, possibly against endogenous bacteria. Standard therapy is therefore directed towards suppression of this immune response. An alternative theory of pathogenesis accounts for epidemiologic and pathophysiologic observations that have been hitherto underemphasized, namely, (1) genetic disorders with deficiencies in neutrophil function can give rise to a clinical and pathologic syndrome indistinguishable from Crohn's; (2) abnormal neutrophil function is well described in Crohn's disease; (3) a group of bacteria implicated in other chronic inflammatory disorders causes impairment of neutrophil function; and (4) 20th century environmental risk factors for Crohn's disease may directly suppress neutrophil function and may have led to a shift in the dominant gut flora with similar effects. We propose that some cases of Crohn's disease result from the interaction of environmental and genetic influences leading to impaired mucosal neutrophil function, resulting in failure to effectively clear intramucosal microbes effectively. While encompassing existing data, this hypothesis proposes a proximate defect in the mucosal immune response. If this paradigm were correct, new therapeutic approaches might involve strategies to alter intestinal flora and stimulate neutrophil function.

Crohn Disease↗
PubMed2001

Plasma cells: finding new light at the end of B cell development.

Plasma cells are cellular factories devoted entirely to the manufacture and export of a single product: soluble immunoglobulin (Ig). As the final mediators of a humoral response, plasma cells play a critical role in adaptive immunity. Although intense effort has been devoted to studying the regulation and requirements for early B cell development, little information has been available on plasma cells. However, more recent work-including studies on genetically altered mice and data from microarray analyses-has begun to identify the regulatory cascades that initiate and maintain the plasma cell phenotype. This review will summarize our current understanding of the molecules that regulate commitment to a plasma cell fate and those that mediate plasma cell function.

Animals↗
PubMed2002

A role for antigen in the maintenance of immunological memory.

The immune system has a memory that it exhibits in the enhanced and augmented responses the second time it meets an antigen. The memory is the result of a number of changes to the system brought about during the primary response. The most important of these changes is the formation of an expanded pool of antigen-specific memory cells. One of the enduring questions in immunology is how these memory cells are maintained for such long periods.

Animals↗
PubMed2006

Regulation of MHC class II expression, a unique regulatory system identified by the study of a primary immunodeficiency disease.

Major histocompatibility complex class II (MHC-II) molecules are of central importance for adaptive immunity. Defective MHC-II expression causes a severe immunodeficiency disease called bare lymphocyte syndrome (BLS). Studies of the molecular defects underlying BLS have been pivotal for characterization of the regulatory system controlling the transcription of MHC-II genes. The precisely controlled pattern of MHC-II gene expression is achieved by a very peculiar and highly specialized molecular machinery that involves the interplay between ubiquitous DNA-binding transcription factors and a highly unusual, tightly regulated, non-DNA-binding coactivator called the MHC class II transactivator (CIITA). CIITA single handedly coordinates practically all aspects of MHC-II gene regulation and has therefore been dubbed the master controller of MHC-II expression. Several of the unusual features of the MHC-II regulatory system may be a consequence of the fact that CIITA originated from an ancient family of cytoplasmic proteins involved in inflammation and innate immunity. The function of CIITA in transcriptional regulation of MHC-II genes could thus be a recent acquisition by an ancestral protein having a role in an unrelated system.

Animals↗
PubMed2005

Airway inflammatory and immunological events in a rat model exposed to toluene diisocyanate.

To investigate the inflammatory and immunological events in the airway induced by a short period of repeated exposure to toluene diisocyanate (TDI), an animal model was established, which resembled the industrial field exposure. After whole body exposure of Wistar rats to 0.38 and 1.20 ppm TDI vapor 4h a day for five consecutive days in a glass chamber, bronchoalveolar lavage (BAL) was performed. BAL fluid cellular and cytokine contents were then determined. Histopathological examinations were also carried out on the lungs. The TDI vapor exposure resulted in airway symptoms similar to those in occupational asthma. BAL fluid cellular analysis and lung histopathological examination revealed that inflammatory response was characterized by marked eosinophil infiltration of the airways. The cytokine assay revealed significant production of IL-4 in the airways of the TDI exposed rats as compared to the control rats. These findings indicated that a short period of repeated exposure to TDI vapor may cause respiratory hypersensitivity in which airway inflammatory and immunological events represented by eosinophil infiltration and Th2 cytokines may play an important role. Also, this animal model may be suitable for exploring the mechanism underlying TDI-induced occupational asthma.

Administration, Inhalation↗
PubMed1979

[Correlation between brain lesion lateralization and immunologic indices in a model of experimental allergic encephalomyelitis].

The report contains new data, concerning checking of concepts of interdependence in the reaction development of humoral and cellular immunity from the lateralization of the affected hemisphere (Chuprikov, 1974). A comparative analysis of immunological indices in a local affections of different cortical zones detected that the influence of regulating mechanisms on the cortical level is accompanied by less expressed effects than on the behalf of the hypothalamo-limbic structures. The dominating influence of the left hemisphere was expressed on the development of humoral antibrain reactions while the right hemisphere demonstrated a prevalent influence on the development of reactions of a retarded type to normal and encephalitogenic antigens from the brain.

Animals↗
PubMed1978

Immunologic abnormalities in an animal model of chronic hypoplastic marrow failure induced by busulfan.

The immunology of chronic hypoplastic marrow failure (CHMF, aplastic anemia) was studied in an experimental murine model of the disease induced by busulfan. B lymphocytes of peripheral blood, spleen, and bone marrow were reduced to 30%-40% and T lymphocytes of thymus, spleen, marrow, and blood were decreased to 20%-70% of control values. IgG and IgM antibody titer to sheep red blood cells were reduced to one-third of control levels, and splenic IgG, but not IgM, plaque-forming cells were fewer on day 7 after antigen stimulation. The proliferative responses to phytohemagglutinin or concanavalin A were reduced in cultures of peripheral blood lymphocytes, splenic lymphocytes, and thymocytes, and cutaneous delayed-type hypersensitivity induced by dinitrofluorobenze was not detected in mice with CHMF. The results demonstrate disturbance of a variety of cellular and humoral functions and suggest that the disturbance was due to quantitative and possibly qualitative abnormalities of the cell types subserving these functions. The results suggest that residual cell injury, the lesion underlying experimental CHMF, is not confined to the myeloid stem cell but also involved cells of the lymphoid series.

Anemia, Aplastic↗
PubMed1980

Biologic and immunologic studies on a murine model of regional lymph node metastasis.

Some biologic, hematologic, and immunologic aspects of the growth and metastasis of the MC-2 fibrosarcoma indicated its suitability as a model for the study of lymphogenous metastasis. The tumor was maintained in syngeneic female BALB/c mice by the serial sc passage of 10(5) viable tumor cells. It metastasized macroscopically in all mice to regional lymph nodes (RLN) and to the lungs. Both forward and retrograde node-to-node metastases were found. Tumor growth and metastasis were associated with splenomegaly, thymus atrophy, cachexia, neutrophilia, lymphopenia, and anemia. Tumor excision at various times after inoculation showed that all mice whose tumors were excised when there was histologic evidence of metastasis in all RLN (day 13; mean of tumor wt, 122 mg) died subsequently from metastases, whereas no animals died whose tumors were excised on or before day 8 (mean of tumor wt, 15 mg). The onset of metastasis was seen in some RLN on day 8. All survivors were immune to challenge with 10(5) viable tumor cells, which demonstrated the immunogenicity of the tumor. Concomitant tumor immunity could be demonstrated prior to the onset of metastasis (days 6 and 7) but not early (days 0--2) or late (days 15, 19, and 20) in primary-site tumor growth. The early immune response to the tumor demonstrable as concomitant tumor immunity appeared to be abrogated by the progressive growth and metastasis of the neoplasm. Tumor cells passaged in adult thymectomized, X-irradiated, syngeneic recipients produced larger RLN metastases and smaller primary tumors than those passaged in control mice.

Animals↗