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Query: UMLS:C0019693 (
HIV
)
170,526
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Dendritic cells have been isolated from the epidermis, dermis, and lymphatics of skin. Cells from each cutaneous compartment can exhibit the distinct morphology, surface phenotype, and strong T-cell-stimulating activity of dendritic cells that are isolated from other organs. Of importance are the mechanisms by which the maturation and movement of dendritic cells are regulated within intact tissues. Epidermal dendritic cells turn over slowly in the steady state. Stimuli, including contact allergens and transplantation, perhaps by inducing a release of cytokines such as granulocyte macrophage-colony-stimulating factor, mobilize these dendritic cells into the dermis and lymph. This migration is accompanied by the maturation of dendritic cell functions; e.g., antigen-presenting
major histocompatibility complex
molecules and B7 costimulators increase markedly. On the other hand, there is a sizable, steady-state flux of dendritic cells in afferent lymph draining the skin, which suggests a constant traffic through the dermis that is independent of sessile epidermal dendritic cells. When explants of skin are placed in organ culture, dendritic cells emigrate into the medium for 1-3 d. The dendritic cells are mature and can bind tightly to small memory T cells that also migrate in these cultures. The emigrated mixtures of dendritic cells and T cells should be useful in the study of many clinical states. This is illustrated by recent experiments showing that migratory skin cells are readily infected with human immunodeficiency virus (HIV)-1. A strong productive infection takes place in the absence of exogenous cytokines, foreign sera, or mitogens or antigens. The dendritic cell-T-cell conjugates are the essential site for infection. This cellular milieu may model events during the sexual transmission of HIV-1, where relevant mucosal surfaces are covered by skin-like epithelia. The capture of CD4+ memory T cells by dendritic cells may explain the chronic drain of immune memory in
HIV infection
.
...
PMID:Maturation and migration of cutaneous dendritic cells. 761 92
Viral variation has been proposed to play a role in the pathogenesis of human immunodeficiency virus type-1 (HIV-1) infection, and is an important consideration in vaccine design. During the course of an infection, isolates with sequence changes in CD8 T-cell and B-cell epitopes arise. To determine whether sequence variation within the V3 loop of
HIV
-1 gp120 affects HLA-DR beta 1*0101-restricted CD4 T-cell recognition, we have generated CD4 T-cell clones (TLC) specific to gp120 V3 loop peptides. Four HLA-DR beta 1*0101-restricted groups of TLC were defined by distinct patterns of responses to a panel of peptides, consistent with a highly diverse T-cell repertoire recognizing the 30 amino acid stretch (296-326) of the gp120 V3 loop. Nevertheless, a single residue change at position 311 was found to abolish the recognition of two of the four groups of TLC. This was not due to an effect of the residue at 311 on binding to
major histocompatibility complex
(
MHC
), because: (1) irrespective of the residue at 311, peptides competed well with the influenza haemagglutinin peptide 307-319 for binding to cell-bound DR1; and (2) R311-specific TLC were also HLA DR beta 1*0101 restricted. Instead, the substitution of arginine for serine at position 311 blocked the interaction of the peptide with the T-cell receptor. Thus, despite the diversity of the T-cell response to the V3 loop of
HIV
-1, a single amino acid change can have a considerable influence on the responding T-cell population. As residue 311 is one of the most variable of the V3 loop residues, these results suggest that CD4 recognition can also exert pressure on viral variation consistent with a role for these cells in antiviral immunity.
...
PMID:The effect of a single amino acid substitution within the V3 loop of HIV-1 gp120 on HLA-DR1-restricted CD4 T-cell recognition. 764 8
Muscle biopsies from 21 dermatomyositis (DM) and 7 polymyositis (PM) patients were studied by conventional histoenzymatic reactions and immunoreacted with antibodies against T cells and subsets, B cells, macrophages, activated T cells, proliferating cells, transferrin and IL-2 receptors, and natural killer cells. The expression of both class I and II molecules from the
major histocompatibility complex
(
MHC
) was also tested. As control groups we used muscle biopsies from normal healthy people, from chronic alcoholics and from a cohort of
HIV
-1 infected patients. In DM cases, severe muscle fiber necrosis, predominant perivascular infiltrates, fibrosis and perifascicular atrophy were the rule whereas in PM cases, endomysial infiltrates and the existence of partially invaded non-necrotic cells were more frequent. Perivascular B cells were found only in some DM cases. Transferrin and IL-2 receptors, proliferating cells and NK cells were detected in some cases from both diseases. MHC class I molecules were detected mainly in perifascicular fibres in DM while in PM the stronger expression was demonstrated in non-necrotic partially invaded cells, suggesting for the latter a
MHC
-restricted T-cell cytotoxicity.
MHC
Class II molecules expression in endothelial cells was detected in a variable fashion in both diseases, probably reflecting different stages of activation of such cells.
...
PMID:Idiopathic inflammatory myopathies. Immunohistochemical analysis of the major histocompatibility complex antigen expression, inflammatory infiltrate phenotype and activation cell markers. 767 62
T-cell epitopes are now well understood as amino-acid nonamers binding to
major histocompatibility complex
molecules. Powerful methods have been developed for their identification through screening of recombinant and synthetic peptides. Multiple epitopes from a single protein are valuable for detecting T-cell reactivity in disease, currently in
human immunodeficiency virus infection
, and in the future in autoimmune disease. Surprises are likely to be encountered while exploring the T-cell repertoire in this way, such as positive as well as negative selection of self-reactivity. T-epitopes are likely to find important applications in therapy, particularly in down-regulation of the immune response. Multiple mechanisms of down-regulation appear to operate, among which bystander suppression by TGF beta-producing T-cells from the gut is of great current interest.
...
PMID:Where are peptides taking us in T-cell biology? 768 73
To investigate whether HTLV-I infection,
HIV
-I infection, or
HIV
-I infection of HTLV-I-infected cells affect the expression of cellular surface molecules, an HTLV-I-infected T cell line derived from the H9 T cell line was established (H36). H9 cells uninfected or infected with HTLV-I were then infected with
HIV
-1. We have compared the density of different surface markers on these three infected H9 T cell lines. These markers consist of T cell-specific antigens (CD2, CD3, CD4, and CD8), activated T cell antigens (CD25 and CD71),
major histocompatibility complex
(
MHC
) antigens (class I and II), and adhesion molecules (LFA-1 and ICAM-1). The experiments reported in this article show that chronic HTLV-I infection,
HIV
-1 infection, and
HIV
-1 infection of HTLV-I-infected T cells modulate the expression of several immunologically important cell surface antigens. The nature and the extent of T lymphoid cell phenotypic modulation depend on the infecting virus. Furthermore, HTLV-I and
HIV
-1 interact with each other in the phenotypic modulation of coinfected cells.
...
PMID:Cell surface phenotypic changes induced in H9 T cells chronically infected with HTLV type I or HIV type 1 or coinfected with the two viruses. 773 88
In this study 96 15-mer peptides encompassing the entire sequence of
HIV
-1 gp120 were synthesized and used to immunize BALB/c mice (i) alone or (ii) in conjunction with the T helper cell determinant FISEAIIHVLHSR (FIS) from sperm whale myoglobin, which is well recognized by
major histocompatibility complex
(
MHC
) class II molecules of BALB/c. Of these peptides 39 were immunogenic per se and 57 were not. Out of the 57 non-immunogenic peptides 53 could be rendered immunogenic with the second immunization protocol. With the exception of 4 cases, the anti-peptide antibody titers induced in (ii) were equal (14 cases) or higher (78 cases) than those induced in (i). From the 96 anti-peptide antibodies tested, 12 were able to recognize recombinant gp120 with good antibody titers, a result in agreement with previously identified B cell epitopes from gp120 by anti-peptide antibodies induced with longer peptides conjugated to a carrier protein. Moreover, 4 of the 12 anti-peptide antisera that recognized gp120 were able to neutralize
HIV
-1 infectivity in vitro, showing that the strategy of co-immunization with FIS may afford functional antibodies.
...
PMID:Simple strategy to induce antibodies of distinct specificity: application to the mapping of gp120 and inhibition of HIV-1 infectivity. 773 88
Because of the importance of the envelope glycoprotein (Env) in determining the pathogenicity of
HIV
-1 and the importance of the immune response to Env in controlling virus spread, attempts are being made to study
HIV
-1 Env-directed immunity in primate models. To date
HIV
-1 Env-specific effector T lymphocyte responses have not been demonstrated in virus-infected nonhuman primates. We have previously reported that cynomolgus monkeys can develop a persistent infection with a chimeric simian-human immunodeficiency virus (SHIV) composed of SIVmac239 carrying the
HIV
-1 env, tat, rev, and vpu genes. We now demonstrate that SHIV-infection of another macaque species, the rhesus monkey, generates persistent,
HIV
-1 Env-specific cytolytic T lymphocyte (CTL) responses. These CTL are CD8+ and
major histocompatibility complex
(
MHC
) class I-restricted. The induction of CTL was correlated neither to the virus load nor to the MHC class I haplotypes of the monkeys. The SHIV-infected rhesus monkey can, therefore, now be employed for studying effector T lymphocyte recognition of
HIV
-1 Env.
...
PMID:Human immunodeficiency virus type 1 envelope glycoprotein-specific cytotoxic T lymphocytes in simian-human immunodeficiency virus-infected rhesus monkeys. 774 49
CD4 is a transmembrane glycoprotein expressed on T-lymphocytes. It is a receptor for class II
major histocompatibility complex
(
MHC
) molecules and for the
HIV
envelope glycoprotein gp120. The extracellular portion of CD4 (sCD4) is a rod-shaped molecule consisting of four domains designated D1 through D4. Denaturant-induced unfolding of sCD4 and of isolated CD4 domains, D1D2 and D3D4, was measured using both ultraviolet absorbance and fluorescence difference spectroscopy. Though both absorbance and fluorescence changes arise from changes in the solvent exposure of the intrinsic tryptophan chromophores, the unfolding curves obtained with the two techniques looked very different for sCD4 and D3D4. This dissimilarity is indicative of a greater than two-state unfolding mechanism. The global three-state fit for sCD4, which simultaneously fit both absorbance and emission data to a model with one thermodynamically stable unfolding intermediate, was significantly better than the best two-state fit, suggesting that there are two unfolding regions. Unfolding of isolated D3D4 also fit a three-state model while unfolding of isolated D1D2 fit satisfactorily to a two-state model. The unfolding of these two isolated fragments could not be summed to yield the unfolding profile of sCD4, implying that an interaction between D2 and D3 is lost by splitting sCD4 between these domains. The unfolding data of isolated D1D2 and D3D4 were used with the solvent-accessible surface area of tryptophans calculated from atomic crystal structure coordinates of human D1D2 and rat D3D4 to assign the unfolding steps. The data are consistent with a model for sCD4 unfolding wherein the one stable intermediate appears to contain only the D4 domain unfolded. The remaining three domains apparently unfold as a unit. Furthermore, interactions between domains D1, D2, and D3 appear to stabilize D4, suggesting that stabilizing interactions exist between D3 and D4 even though the unfolding of the D3D4 fragment is best fit by a three-state model. This report is the first to describe a thermodynamic basis for a wide range of biological properties implicated for CD4.
...
PMID:Interdomain communication of T-cell CD4 studied by absorbance and fluorescence difference spectroscopy measurements of urea-induced unfolding. 775 78
Langerhans cells (LC), the dendritic antigen presenting cells of the skin, mature into potent immunostimulatory cells during migration to regional lymph nodes, where they are identified as interdigitating cells (IDC). Since mature Langerhans cells (mLC) resemble IDC in phenotype and immunostimulatory capacity, we examined whether these cells were susceptible to infection with macrophagetropic and lymphotropic strains of human immunodeficiency virus type 1 (HIV-1). Highly purified cell preparations of mLC migrating from human epidermis expressed high amounts of
major histocompatibility complex
(
MHC
) class I and II antigens and of the accessory molecules CD40, CD80 and CD86, indicative of the phenotype of potent immunostimulatory cells. CD4 expression was upregulated on mLC during cultivation, independent of the presence of tumour necrosis factor alpha (TNF-alpha) and granulocyte-macrophage colony-stimulating factor (GM-CSF) in the culture medium. The macrophagetropic
HIV
-1 strain SF162 replicated to higher titres in mLC than the lymphotropic strain IIIB. Both strains induced syncytia, with SF162 showing a more rapid cytopathic effect. Addition of TNF-alpha enhanced virus production, due to better cell viability under TNF-alpha treatment, whereas GM-CSF did not significantly influence viability of cells and replication pattern of the virus. These findings suggest that in the infected individual IDC in lymph nodes may function as target cells for
HIV
-1.
...
PMID:Replication pattern of human immunodeficiency virus type 1 in mature Langerhans cells. 778 62
Based on our findings that
HIV
-1 (human immunodeficiency virus type 1) soluble gp41 (sgp41; amino acids 539-684) bound to human T, B, and monocyte cells and enhanced
major histocompatibility complex
(
MHC
) class I and II antigen expression on Raji cells, we examined the effect of
HIV
-1 sgp41 on the surface expression of
MHC
I and II, ICAM-1, and CD4 molecules on human H9 and U937 cells. Flow cytometry (FACS) analysis demonstrated that sgp41 selectively enhanced MHC class I expression by about 75% on H9 cells and by about 85% on U937 cells, while the ICAM-1 expression was increased by about 70% only on H9 cells and remained unaltered on U937 cells; other molecules, such as MHC class II and CD4, remained unaltered. By comparison, alpha-, beta-, and omega-interferons, but not gamma-interferon, showed similar effects as sgp41 on the expression of MHC class I and ICAM-1 on H9 and U937 cells. The results suggest that
HIV
-1 gp41 may have a biological function that is involved in the regulation of human MHC class I and ICAM-1 expression.
...
PMID:HIV-1 gp41 enhances major histocompatibility complex class I and ICAM-1 expression on H9 and U937 cells. 791 56
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