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Showing papers in "Immunity in 1999"


Journal ArticleDOI
01 Oct 1999-Immunity
TL;DR: It is demonstrated that TLR2 and TLR4 recognize different bacterial cell wall components in vivo andTLR2 plays a major role in Gram-positive bacterial recognition.

3,364 citations


Journal ArticleDOI
01 Aug 1999-Immunity
TL;DR: It is suggested that PD-1 is involved in the maintenance of peripheral self-tolerance by serving as a negative regulator of immune responses in lymphocytes and monocytic cells following activation.

2,465 citations


Journal ArticleDOI
01 Jul 1999-Immunity
TL;DR: It is demonstrated that MyD88 knockout mice lack the ability to respond to LPS as measured by shock response, B cell proliferative response, and secretion of cytokines by macrophages and embryonic fibroblasts, and the inability of MyD 88 knockout mice to induce LPS-dependent gene expression cannot be attributed to lack of the activation of MAP kinases and NF-kappaB.

2,135 citations


Journal ArticleDOI
01 Jan 1999-Immunity
TL;DR: Findings provide evidence that constitutively activated Stat3 signaling contributes to the pathogenesis of multiple myeloma by preventing apoptosis.

1,682 citations


Journal ArticleDOI
01 May 1999-Immunity
TL;DR: It is suggested that Notch1 plays an obligatory and selective role in T cell lineage induction in mice with a neonatally induced loss of Notch 1 function.

1,442 citations


Journal ArticleDOI
01 Mar 1999-Immunity
TL;DR: Development of two specific pathologies in mutant mice, i.e., chronic inflammatory arthritis and Crohn's-like inflammatory bowel disease, suggests that defective function of ARE may be etiopathogenic for the development of analogous human pathologies.

1,347 citations


Journal ArticleDOI
01 Jan 1999-Immunity
TL;DR: Taken together, Stat3 plays a critical role in deactivation of macrophages and neutrophils mainly exerted by IL-10, which contributes to chronic enterocolitis with age.

1,231 citations


Journal ArticleDOI
01 Sep 1999-Immunity
TL;DR: The results suggest that Notch1 provides a key regulatory signal in determining T lymphoid versus B lymphoid lineage decisions, possibly by influencing lineage commitment from a common lymphoid progenitor cell.

1,021 citations


Journal ArticleDOI
01 Dec 1999-Immunity
TL;DR: A substantial minority of inflammatory monocytes carry phagocytosed particles to lymph nodes and differentiate into DCs, and this transport was reduced by more than 85% in monocyte-deficient osteopetrotic mice.

947 citations


Journal ArticleDOI
01 Jun 1999-Immunity
TL;DR: Subpopulations of CTL and NK cells may be uniquely suited for combating HIV, and evidence that HIV-1 selectively downregulates HLA-A andHLA-B but does not significantly affect H LA-C or HLAE is presented.

888 citations


Journal ArticleDOI
01 Apr 1999-Immunity
TL;DR: It is suggested that CD8+CTL are better correlated with protection against HCV infection than antibodies, and every specificity shown during acute hepatitis persisted in normal liver tissue more than 1 yr after resolution.

Journal ArticleDOI
01 Jan 1999-Immunity
TL;DR: Interleukin-18 binding protein functions as an inhibitor of the early Th1 cytokine response, suggesting that viral products may attenuate IL-18 and interfere with the cytotoxic T cell response.

Journal ArticleDOI
01 Aug 1999-Immunity
TL;DR: Evidence is provided that the self-peptides controlling positive selection in the thymus serve to maintain the longevity of mature T cells in the periphery, when total T cell numbers are reduced, these self-ligands become overtly stimulatory and cause naive T cells to proliferate and undergo homeostatic expansion.

Journal ArticleDOI
01 Apr 1999-Immunity
TL;DR: Mice reconstituted with CXCR4-deficient fetal liver cells have reduced donor-derived mature B lymphocytes in blood and lymphoid organs and the numbers of pro-B and pre-B cells are reduced in bone marrow and abnormally high in blood.

Journal ArticleDOI
01 Apr 1999-Immunity
TL;DR: The role of B cells as the secretion of arthritogenic immunoglobulins is identified in rheumatoid arthritis and it is suggested that a similar scenario may unfold in some other arthritis models and in human patients, beginning with pervasive T cell autoreactivity and ending in immunoglobeulin-provoked joint destruction.

Journal ArticleDOI
01 Feb 1999-Immunity
TL;DR: GeGeilen, S.C. Runkel, and N.C Runkel as mentioned in this paper provided comments on this review and they would like to thank Drs. Geilen and S.


Journal ArticleDOI
01 Jun 1999-Immunity
TL;DR: The telomerase catalytic subunit (hTERT) is characterized as a widely expressed TAA capable of triggering antitumor cytotoxic T lymphocyte (CTL) responses and identified as a potentially important and widely applicable target for anticancer immunotherapeutic strategies.

Journal ArticleDOI
01 Feb 1999-Immunity
TL;DR: Rac2-deficient mice were created to define the physiological requirement for two near-identical Rac proteins in hematopoietic cells, and showed significant defects in chemotaxis, in shear-dependent L-selectin-mediated capture on the endothelial substrate Glycam-1, and in both F-actin generation and p38 and p42/p44 MAP kinase activation induced by chemoattractants.

Journal ArticleDOI
01 Mar 1999-Immunity
TL;DR: The Ikaros gene family encodes zinc finger DNA-binding proteins essential for lineage determination and control of proliferation in the lymphoid system that are capable of targeting chromatin remodeling and deacetylation complexes in vivo, and it is proposed that the restructuring of chromatin is a key aspect of Ikaro function in lymphocyte differentiation.

Journal ArticleDOI
01 Apr 1999-Immunity
TL;DR: It is indicated that IKK-beta is crucial for liver development and regulation of NF-kappaB activity and that Ikk-alpha can only partially compensate for the loss of IKK, while basal and cytokine-inducible kinase activities of the IKK complex are greatly reduced.

Journal ArticleDOI
01 Aug 1999-Immunity
TL;DR: In this paper, the authors examined the molecular interactions required for peripheral CD8+ T cell expansion in lymphopenic mice without conventional antigenic stimulation and found that the expansion of T cells in lymph openic hosts was peptide specific.

Journal ArticleDOI
01 Feb 1999-Immunity
TL;DR: It is demonstrated that, while lymphoid development is normal, Stat5a/b mutant peripheral T cells are profoundly deficient in proliferation and fail to undergocell cycle progression or to express genes controlling cell cycle progression.

Journal ArticleDOI
01 Mar 1999-Immunity
TL;DR: To probe the role of LAT in T cell development, the LAT gene was disrupted by targeting and normal B cell populations but the absence of any mature peripheral T cells were revealed.

Journal ArticleDOI
01 Feb 1999-Immunity
TL;DR: Results indicate cathepsin S is a major Ii-processing enzyme in splenocytes and dendritic cells, and its role in humoral immunity critically depends on how antigens access the immune system.

Journal ArticleDOI
01 Jan 1999-Immunity
TL;DR: Mice doubly deficient in both enzymes formed massive abscesses containing commensal organisms, mostly enteric bacteria, even when reared under specific pathogen-free conditions with antibiotics, establishing the existence of a mechanism of macrophage antibacterial activity independent of phox and NOS2.

Journal ArticleDOI
01 Apr 1999-Immunity
TL;DR: The data reveal a narrowing of the secondary repertoire relative to the primary repertoire, largely resulting from the loss of cells expressing TCRs with the fastest dissociation rates for peptide/MHC binding.

Journal ArticleDOI
01 Oct 1999-Immunity
TL;DR: It is suggested that induction of B7h by TNFalpha may function as a mechanism to directly augment recognition of self during inflammation and define a novel costimulatory ligand for T cells.

Journal ArticleDOI
01 Sep 1999-Immunity
TL;DR: Different IL-2Rbeta chain signaling modules regulate T cell fate by stimulating growth and survival or by promoting apoptosis.

Journal ArticleDOI
01 Jun 1999-Immunity
TL;DR: Results indicate that ROS can regulate signals involved in caspase activation and apoptosis and may contribute to peripheral T cell deletion.