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Results: 181 to 187 of 187

Publication Record


Regulatory defects in Cbl and mitogen-activated protein kinase (extracellular signal-related kinase) pathways cause persistent hyperexpression of CD40 ligand in human lupus T cells.
Yi Y, McNerney M, Datta SK
(2000) J Immunol 165: 6627-34
MeSH Terms: Abatacept, Adolescent, Adult, Antigens, CD, Antigens, Differentiation, CD28 Antigens, CD40 Ligand, CTLA-4 Antigen, Calcineurin, Cell Line, Clonal Anergy, DNA-Binding Proteins, Enzyme Activation, Female, Humans, Immunity, Innate, Immunoconjugates, Immunologic Memory, Interleukin-2, Lupus Erythematosus, Systemic, MAP Kinase Signaling System, Male, Middle Aged, Mitogen-Activated Protein Kinases, NFATC Transcription Factors, Nuclear Proteins, Phosphorylation, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-cbl, Receptors, Antigen, T-Cell, T-Lymphocytes, T-Lymphocytes, Helper-Inducer, Transcription Factors, Tyrosine, Ubiquitin-Protein Ligases
Show Abstract · Added March 5, 2014
To identify intrinsic defects in lupus, we studied short-term, CD4(+) T cell lines that were established from 16 lupus patients (active or inactive) and 15 normal subjects by stimulating once with anti-CD3, anti-CD28, and IL-2. After resting, the pure CD4(+) T cells were exposed to anergy-inducing stimulation with plate-bound anti-CD3 mAb in the absence of APC. Lupus T cells showed prolonged high level expression of CD40 ligand (CD40L, CD154) even in the face of anergy protocol, which shut down CD40L expression in normal T cells. The sustained CD40L expression in lupus T cells did not correlate with memory status or Th deviation, and was relatively independent of IL-2 or other autocrine or paracrine signals via CD28 or CTLA-4. Cyclosporin A could block CD40L expression by lupus T cells when added early during the anti-CD3 stimulation period, but only partially when added later, indicating that another mechanism regulates the prolonged hyperexpression of CD40L besides the Ca(2+) --> calcineurin-dependent NF-AT pathway. When exposed to the anergy protocol, lupus T cells, in marked contrast to normal T cells, did not phosphorylate Cbl/Cbl-b but continued to express strongly phosphorylated extracellular signal-regulated kinase (ERK); U0126, a specific inhibitor of mitogen-activated protein kinase kinase --> ERK, could block both the early and the prolonged hyperexpression of CD40L. Thus, pathways regulating the activities of Cbl and one particular mitogen-activated protein kinase, ERK, are involved in the prolonged hyperexpression of CD40L in lupus T cells.
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35 MeSH Terms
Regulation of intestinal alpha-defensin activation by the metalloproteinase matrilysin in innate host defense.
Wilson CL, Ouellette AJ, Satchell DP, Ayabe T, López-Boado YS, Stratman JL, Hultgren SJ, Matrisian LM, Parks WC
(1999) Science 286: 113-7
MeSH Terms: Amino Acid Sequence, Animals, Catalysis, Cytoplasmic Granules, Escherichia coli, Escherichia coli Infections, Female, Humans, Immunity, Innate, Immunity, Mucosal, Intestinal Mucosa, Intestine, Small, Male, Matrix Metalloproteinase 7, Metalloendopeptidases, Mice, Molecular Sequence Data, Paneth Cells, Protein Precursors, Recombinant Fusion Proteins, Salmonella typhimurium, Tissue Extracts
Show Abstract · Added August 13, 2010
Precursors of alpha-defensin peptides require activation for bactericidal activity. In mouse small intestine, matrilysin colocalized with alpha-defensins (cryptdins) in Paneth cell granules, and in vitro it cleaved the pro segment from cryptdin precursors. Matrilysin-deficient (MAT-/-) mice lacked mature cryptdins and accumulated precursor molecules. Intestinal peptide preparations from MAT-/- mice had decreased antimicrobial activity. Orally administered bacteria survived in greater numbers and were more virulent in MAT-/- mice than in MAT+/+ mice. Thus, matrilysin functions in intestinal mucosal defense by regulating the activity of defensins, which may be a common role for this metalloproteinase in its numerous epithelial sites of expression.
1 Communities
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22 MeSH Terms
Contribution of the innate immune system to autoimmune diabetes: a role for the CR1/CR2 complement receptors.
Noorchashm H, Moore DJ, Lieu YK, Noorchashm N, Schlachterman A, Song HK, Barker CF, Naji A
(1999) Cell Immunol 195: 75-9
MeSH Terms: Animals, B-Lymphocytes, Complement C3, Diabetes Mellitus, Type 1, Immunity, Innate, Immunophenotyping, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Inbred NOD, Receptors, Complement 3b, Receptors, Complement 3d, Spleen
Show Abstract · Added October 24, 2013
B lymphocytes are required for diabetogenesis in nonobese diabetic (NOD) mice. The complement component of the innate immune system regulates B cell activation and tolerance through complement receptors CR1/CR2. Thus, it is important to assess the contribution of complement receptors to autoimmune diabetes in NOD mice. Examination of the lymphoid compartments of NOD mice revealed striking expansion of a splenic B cell subset with high cell surface expression of CR1/CR2. This subset of B cells exhibited an enhanced C3 binding ability. Importantly, long-term in vivo blockade of C3 binding to CR1/CR2 prevented the emergence of the CR1/CR2(hi) B cells and afforded resistance to autoimmune diabetes in NOD mice. These findings implicate complement as an important regulatory element in controlling the T cell-mediated attack on islet beta cells of NOD mice.
Copyright 1999 Academic Press.
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13 MeSH Terms
CCR5 genotype and resistance to vertical transmission of HIV-1.
Philpott S, Burger H, Charbonneau T, Grimson R, Vermund SH, Visosky A, Nachman S, Kovacs A, Tropper P, Frey H, Weiser B
(1999) J Acquir Immune Defic Syndr 21: 189-93
MeSH Terms: Alleles, Anti-HIV Agents, Child, Female, Genotype, HIV Infections, HIV-1, Humans, Immunity, Innate, Infectious Disease Transmission, Vertical, Prospective Studies, Receptors, CCR5, Reverse Transcriptase Inhibitors, Zidovudine
Show Abstract · Added March 5, 2014
A human gene has been identified that affects susceptibility to HIV-1 infection. The gene codes for CCR5, the coreceptor for macrophage-tropic strains of HIV-1. Individuals who are homozygous for a deleted, mutant form of the gene, delta32, display a high degree of natural resistance to sexual and parenteral transmission of HIV-1. To investigate whether delta32 plays a role in vertical transmission, we determined the CCR5 genotype of 552 children born to infected mothers in the United States and correlated the genotypes with HIV-1 infection status. Of these children, 13% were white, 30% Latino, and 56% African American, reflecting the ethnic makeup of infected women in the United States. The delta32 gene frequency varied among these groups, ranging from 0.08 in whites to 0.02 in both Latinos and African Americans. Approximately 27% of the children in each ethnic group were infected. Four children were identified as delta32 homozygotes, two uninfected whites (3.77%) and two uninfected Latinos (1.68%). None of the infected children displayed the delta32 homozygous genotype. Among Latinos and whites, the number of uninfected children who carried the homozygous delta32 mutation was significantly greater than that predicted by the Hardy-Weinberg equilibrium (p < .001 for Latinos, p = .044 for whites). This association was noted in Latino and white children whose mothers were either treated or untreated with zidovudine. These data document the occurrence of the homozygous delta32 genotype among children of HIV-1-infected mothers and suggest that this mutant genotype may confer protection from mother-to-child transmission of HIV-1. They also suggest that sexual, parenteral, and vertical transmission all involve processes that use CCR5 as a coreceptor for primary HIV-1 infection. Therefore, blocking the CCR5 receptor may provide an additional strategy to prevent HIV-1 vertical transmission.
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14 MeSH Terms
T cell-independent response to Brucella-insulin identifies a preimmune repertoire for insulin.
Thomas JW, Kralick PM, Ewulonu UK
(1997) J Immunol 159: 2334-41
MeSH Terms: Amino Acid Sequence, Animals, Antibodies, Bacterial, Antibodies, Monoclonal, Antibody Affinity, Antibody Specificity, Antigens, T-Independent, B-Lymphocyte Subsets, Base Sequence, Brucella abortus, Gene Rearrangement, B-Lymphocyte, Genes, Immunoglobulin, Immunity, Innate, Immunoglobulin Heavy Chains, Immunoglobulin Variable Region, Immunoglobulin kappa-Chains, Immunologic Memory, Insulin, Insulinoma, Mice, Mice, Inbred BALB C, Molecular Sequence Data, Pancreatic Neoplasms, Rats, Sequence Alignment, Sequence Homology, Specific Pathogen-Free Organisms
Show Abstract · Added November 6, 2013
An early or preimmune repertoire for anti-insulin B cells was examined using the T cell-independent (TI) response to insulin conjugated to Brucella abortus (BA-ins). mAbs from the BA-ins response reflect a repertoire present 7 to 10 days before the first Ab-forming cells (AFC) are detected in primary T cell-dependent (TD) responses to insulin. Although 4 of 6 BA-ins mAb express IgG2 isotype, evidence for somatic mutation is limited. A total of 9 of 12 V regions are identical with known V(H) or Vkappa genes, and consensus sequences suggest two other V genes may be in germ-line configuration. The relative avidities (50% inhibition of binding) of TI anti-insulins cover a broad range and are consistent with a germ-line anti-insulin repertoire that is functionally diverse. The V(H)s of 5 mAb are from two subsets of J558 genes (205.1 and 186.3) that dominate the B cell pool of adult mice and are different from the V(H)s used by anti-insulin mAb in primary TD responses. One IgM anti-insulin (mAb 301) uses V(H)-J606 and Vkappa1, and this mAb binds beta cells. Other TI mAb use either Vkappa5 or Vkappa19.3 genes and are similar to Vkappa genes used by anti-insulin mAb from TD responses. The data show that mutations in germ-line genes are not required for measurable insulin binding by monospecific mAb from adult mice. The recurrent use of Vkappa genes in both early (TI response) and late (TD responses) suggest that these structures are important in insulin binding.
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27 MeSH Terms
CD1d1 mutant mice are deficient in natural T cells that promptly produce IL-4.
Mendiratta SK, Martin WD, Hong S, Boesteanu A, Joyce S, Van Kaer L
(1997) Immunity 6: 469-77
MeSH Terms: Animals, Antigens, CD1, Cell Differentiation, Immunity, Innate, Immunoglobulin E, Interleukin-4, Liver, Lymphocyte Count, Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Receptors, Antigen, T-Cell, Spleen, T-Lymphocyte Subsets, Thymus Gland
Show Abstract · Added December 10, 2013
Murine CD1 has been implicated in the development and function of an unusual subset of T cells, termed natural T (NT) cells, that coexpress the T cell receptor (TCR) and the natural killer cell receptor NK1.1. Activated NT cells promptly produce large amounts of IL-4, suggesting that these cells can influence the differentiation of CD4+ effector T cell subsets. We have generated mice that carry a mutant CD1d1 gene. NT cell numbers in the thymus, spleen, and liver of these mice were dramatically reduced. Activated splenocytes from mutant mice did not produce IL-4, whereas similarly treated wild-type splenocytes secreted large amounts of this cytokine. These results demonstrate a critical role for CD1 in the positive selection and function of NT cells.
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15 MeSH Terms
The origin of the autoimmune disease-resistant LER rat: an outcross between the buffalo and autoimmune disease-prone Lewis inbred rat strains.
Goldmuntz EA, Wilder RL, Goldfarb Y, Cash JM, Zha H, Crofford LJ, Mathern P, Hansen CT, Remmers EF
(1993) J Neuroimmunol 44: 215-9
MeSH Terms: Alleles, Animals, Autoimmune Diseases, Base Sequence, Crosses, Genetic, Immunity, Innate, Molecular Sequence Data, Oligodeoxyribonucleotides, Polymorphism, Genetic, Rats, Rats, Inbred ACI, Rats, Inbred BUF, Rats, Inbred F344, Rats, Inbred Lew, Rats, Inbred Strains, Repetitive Sequences, Nucleic Acid, Species Specificity
Show Abstract · Added September 18, 2013
The Lewis (LEW) rat strain is highly susceptible to a large number of experimentally induced inflammatory and autoimmune diseases. The Lewis resistant (LER) rat strain, which reportedly arose as a spontaneous mutation in a closed colony of LEW rats, is resistant to many of these disorders. The mechanism of resistance is not yet clear. We report the analysis of 19 simple dinucleotide repeat polymorphisms in 13 rat strains including the LEW/N and LER/N rat strains. The LEW/N and LER/N alleles were the same in only 42% of cases. For all of the other polymorphisms, the LER/N and Buffalo (BUF/N) rat strain alleles were identical. These data provide evidence that the LER strain did not arise as a spontaneous mutation in the LEW strain but is the result of an outcross between the LEW and BUF rat strains. The LER rat strain is now a recombinant inbred rat strain. This information should facilitate the genetic analysis of the loci responsible for resistance to experimental autoimmune disease in the LER rat.
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17 MeSH Terms