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C Agostini

Publications and source records attributed to C Agostini.

At least 73 records · Page 4Linked to original sources
PubMed1996

Immunologic effects of HIV in the lung.

This article covers a selected group of topics dealing with the contribution of lung immunocompetent cells in the host defense mechanisms against HIV. These include recent findings suggesting that bidirectional signals between alveolar macrophages and pulmonary cytotoxic T lymphocytes define regulatory networks, which contribute to the accumulation of HIV-specific effector cells in the lung microenvironment. The authors also emphasize the cell pattern of HIV infection in the lung, highlighting the role of the retrovirus in weakening pulmonary host defenses and its spreading into the lower respiratory tract.

CD4-Positive T-Lymphocytes↗
PubMed1996

IL-12 is involved in the activation of CD3+ granular lymphocytes in patients with lymphoproliferative disease of granular lymphocytes.

We investigated the effects of Il-12 on functional properties of CD3+ CD8+ granular lymphocytes (GL) of of patients with lymphoproliferative disease of granular lymphocytes (LDGL). To this aim, in 10 cases with clonal CD3+ GL proliferation (nine cases with an associated TCR alpha/beta receptor and one case with a TCR gamma/delta receptor) we studied the proliferative and cytotoxic activities of resting and alpha CD3 monoclonal antibody (mAb) activated cells in the presence of rIL-12 and anti-IL-12 blocking antibodies. Specific mRNA for IL-12 p40 subunit was also investigated. Our results showed that rIL-12 increased the proliferation of alpha CD3 pre-stimulated GL (2 to 6 times). Further, anti-IL-12 antibodies partially inhibited alpha CD3-induced cell growth, suggesting a role for this cytokine in the alpha CD3-mediated GL activation. The addition of antibodies blocking the p55 and p75 chains of IL-2 receptor (IL-2R) did not inhibit the rIL-12-mediated cell proliferation, indicating that the activity of rIL-12 is dependent of IL-2 in the in vivo expanded GL of patients under study. Concerning the cytotoxic activity, rIL-12 increased the alpha CD3-mediated NK activity against K-562 target cells and alpha CD3 redirected cytotoxicity against P815 target cells. Molecular analysis pointed out that, following alpha CD3 stimulation, patients' GL increased the expression of specific mRNA for the p40 subunit of IL-12 as compared to baseline conditions. Our data indicate that IL-12 is involved in the mechanisms of activation of clonal CD3+ GL in patients with LDGL; these features are consistent with the possibility that this discrete subset of GL might represent in vivo primed cytotoxic T lymphocytes.

Antibodies, Monoclonal↗
PubMed1996

Lysis of pulmonary fibroblasts by lymphokine (IL-2)-activated killer cells--a mechanism affecting the human lung microenvironment?

In this study we investigated whether IL-2-activated killer cells may bind and exert lytic activity against non-transformed lung fibroblasts. We demonstrated that human lymphokine-activated killer (LAK) cells generated in vitro following incubation with recombinant IL-2 of either peripheral blood mononuclear cells (PB-LAK) or lymphocytes obtained from bronchoalveolar lavage (BAL-LAK), but not resting cells, can lyse normal lung fibroblasts obtained from transbronchial lung biopsies in a 4-h 51Cr release assay. Both autologous and allogeneic fibroblasts were consistently lysed by LAK cells, thus suggesting that the phenomenon we observed is not MHC-restricted. Since fibroblasts can bind IL-2 through specific receptors, we evaluated whether long-term culture with rIL-2 could modulate the susceptibility to lysis of target cells. Our data showed that autologous fibroblasts were more resistant to lysis than allogeneic fibroblasts when they were cultured with rIL-2. Since LAK cells have been demonstrated to release a series of different immunomodulatory cytokines, we evaluated the effect of short-term incubation of fibroblasts with different factors, including IL-1, IL-2, IL-3, IL-4, IL-6, tumour necrosis factor-alpha (TNF-alpha), and interferon-gamma (IFN-gamma), on the binding and the lysis mediated by LAK cells. These cytokines were not directly cytotoxic on fibroblasts. Only IFN-gamma was found to have a significant protective effect against the lysis. Our data support the concept that a self-directed cytotoxicity against pulmonary fibroblasts is generated during lymphocyte activation with rIL-2.

Cells, Cultured↗
PubMed1996

Skewing of the T-cell receptor repertoire in the lung of patients with HIV-1 infection.

OBJECTIVES: A bias of the use of T-cell receptor (TCR) V beta regions has been reported both in peripheral blood and in several tissues in patients with AIDS, including lymph nodes, spleen and salivary glands. Although the disease is frequently characterized by an infiltration of T cells in the lung interstitium, no information is presently available on the configuration of the TCR repertoire in this microenvironment. This study was performed to address the question of whether a bias in T-cell selection occurs in the lung of patients with AIDS. METHODS: TCR beta-chain variable region (TCR-V beta) repertoire was analysed by flow cytometry and polymerase chain reaction (PCR) analyses in blood and lung lymphocytes of 13 patients with HIV-1 infection at different stages of the disease. Blood and lung lymphocytes were also assessed for their responsiveness to different superantigenic stimuli represented by staphylococcal enterotoxins (SEA, SEB, SEC1, SEC2, SED and SEE). RESULTS: Flow cytometry analysis in AIDS patients demonstrated an overexpression of cells bearing V beta 2 and V beta 3 gene segments in the lung compared with peripheral blood of the same subjects, as well as to lung and blood lymphocytes of normal controls. PCR analysis performed in AIDS patients extended these observations and demonstrated a significant bias also in the use of T cells bearing V beta 7 and V beta 9 gene regions in the lung compartment with respect to the blood. Virtually all T cells bearing the overrepresented V beta segment belong to the CD8 subset. Interestingly, T-lymphocyte response to different superantigens demonstrated a low proliferative rate in the lung with respect to the blood in HIV-1-infected patients. CONCLUSIONS: These findings indicate a compartmentalization of cells bearing discrete V beta gene products in the pulmonary microenvironment of patients with AIDS and suggest that the expansion of specific-V beta region subsets occurring in the lung might result from triggering by a superantigen.

Adult↗
PubMed1996

Immunology of idiopathic pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is an immunomediated disorder characterized by a chronic inflammation of the lower respiratory tract, type I epithelial cell damage, accumulation of connective tissue components, fibroblast proliferation, and deposition of matrix proteins. The past few years have seen remarkable advances in the understanding of the immunopathogenesis of IPF. It is becoming clear that, although normal inflammatory reaction in the lung generally resolves, the rapidity and efficiency with which inflammatory constituents are removed from alveolar airspaces is altered in patients with IPF. The loss of the balance between events that mediate resolution or perpetuation of inflammatory responses sets the stage for severe lung injury, tissue remodelling, and the irreversible development of pulmonary fibrosis. This review outlines the complexity of cellular signalling processes taking place in fibrotic lung, providing a bridge between basic research and clinical relevance in the treatment of these patients.

Cell Communication↗
PubMed1996

Expression of tumor necrosis factor-receptor superfamily members by lung T lymphocytes in interstitial lung disease.

Recently, a novel receptor superfamily has been identified whose members interact with a parallel family of ligands showing homology to tumor necrosis factor (TNF). To investigate the role of these receptor structures in the pulmonary environment, we evaluated the expression of some members of the TNF-receptor (CD27, CD30, CD40, CD95/Fas, CD120a, and CD120b) and TNF-ligand (CD40L, CD70/CD27L, CD30L, and mTNFalpha) superfamilies by bronchoalveolar lavage (BAL) T cells recovered from healthy subjects and patients with interstitial lung disease (ILD). Lung T lymphocytes recovered from control subjects showed a slight expression of CD27 but did not bear CD30, CD40, CD120a, or CD120b antigens. CD27 expression was restricted to normal CD4+ cells. Fas antigen (CD95), which is involved in activation-driven T-cell suicide, and the ligand for CD27 (CD70) were weakly expressed by normal BAL T-cell subpopulations. In patients with sarcoidosis, the majority of pulmonary T lymphocytes were CD4+ cells that expressed low levels of CD27 antigen and an upregulation of CD95 and CD70 molecules. When we characterized lymphocytes accumulating in the lung of patients with HIV infection and hypersensitivity pneumonitis, we demonstrated that T cells accounting for the CD8 alveolitis bore TNF-receptor type 2 (CD120b) at high density and were CD70+ while CD40L, CD30L, or mTNF-alpha expression were not found. The discrete surface expression of the TNF-receptors and TNF-ligands on alveolar T-cell subsets suggests that these molecules play a role in the immune regulatory mechanisms that ultimately lead to the alveolitis in the pulmonary microenvironment of interstitial lung disease.

Adult↗
PubMed1996

Lung lymphocytes: origin, biological functions, and laboratory techniques for their study in immune-mediated pulmonary disorders.

Different types of immunocompetent cells, including T lymphocytes and alveolar macrophages, account for pulmonary host defense. Taking advantage of the availability of the monoclonal antibody technique, cell culture facilities, pure recombinant cytokines, and molecular probes for their genes, in the last few years it has been possible to keenly study the different steps that lead to the compartmentalization of immune response in human lung. Furthermore, the immunological analysis of cells retrieved from bronchoalveolar lavage (BAL) allowed recognition of the importance of immune mechanisms in the evolution of immune-mediated pulmonary disorders. The purpose of this review is to summarize recent advances on the immunologic characterization of lung lymphocytes in health and disease. Following a brief description of the pathways through which the pulmonary lymphoid system contributes to removing potentially harmful inhaled antigenic materials, available laboratory techniques to evaluate the lymphoid component of the pulmonary immune system and their byproducts are discussed. These techniques cover methods for preparing lymphocytes from the BAL fluid and for characterizing lung lymphocytes both in cell suspensions and pulmonary tissue biopsies. Other sections of this review describe the techniques for measuring the immunologic effector functions of lung lymphocytes. We also provide the reader with a flavor of the molecular biology methods used to characterize lymphocytes in the pulmonary microenvironment. The final sections of the review article highlight the pathogenetic role envisaged for lymphoid cells in pulmonary disease states and emphasize the importance of the BAL analysis in the clinical management of the most relevant immune-mediated lung disease.

Animals↗
PubMed1995

Analysis of the T cell receptor in the lymphoproliferative disease of granular lymphocytes: superantigen activation of clonal CD3+ granular lymphocytes.

To investigate whether cell populations in CD3+ lymphoproliferative disease of granular lymphocytes (LDGLs) were skewed toward the use of specific V beta regions, we studied the repertoire of T-cell receptor (TCR) V beta gene products in 18 patients, as well as their relationship to the clonal bands in the Southern blot and the activation mediated by superantigens. Using a panel of monoclonal antibodies (mAbs) for conserved V beta segments and PCR, a dominant population expressing a specific V beta region was demonstrated in all patients. In five (27%) cases, granular lymphocytes (GLs) were found to express the V beta 13.1, while V beta 8 and V beta 6 were each expressed in three (17%) cases. The remaining cases were characterized by the proliferation of TCR V beta 2, V beta 3, V beta 4, V beta 9, V beta 12, V beta 16, and V beta 20. This finding indicates a biased usage of a limited TCR V beta in LDGLs, since nearly 60% of the cases utilized only three families of the TCR V beta genes. In all of the cases studied, we proved that the subset recognized by mAb and PCR was identical to that accounting for the extra band(s) of the Southern blot. This finding confirms the clonal nature of the population identified according to TCR V beta expression both by phenotype and PCR. On functional grounds, we evaluated whether GLs can be activated through the specific TCR using the superantigens recognizing discrete V beta families, such as staphylococcal proteins, including SEA, SEB, SEC1, SEC2, SED, and SEE. We demonstrated that the TCR-alpha/beta of clonal GLs in LDGL patients is functionally active in delivering cytotoxic and proliferative signals upon superantigen activation.

CD3 Complex↗
PubMed1995

Immunosuppressive therapy prevents recurrent pericarditis.

OBJECTIVES: This study reviews the clinical outcome of a series of patients with recurrent pericarditis before and after immunosuppressive therapy. BACKGROUND: Despite anti-inflammatory treatment, some patients with acute pericarditis experience repeated relapses of the disease. The use of steroids for the treatment of recurrent pericarditis remains controversial. METHODS: Twelve patients (4 women, 8 men; mean [+/- SD] age 35.9 +/- 17.2 years, range 15 to 65) with recurrent pericarditis unrelated to any systemic disease were selected. All 12 patients previously received ineffective short-term courses of low dose steroids and had a total of 39 relapses during a mean follow-up period of 14.2 months (range 4 to 50). A 3-month course of treatment with prednisone, at an immunosuppressive dosage, was started (1 to 1.5 mg/kg body weight per day for 4 weeks, then gradually withdrawn). When prednisone reduction was undertaken, all patients started a 5-month course of treatment with aspirin (1.6 g/day until steroid suspension, then reduced to 0.8 g/day). RESULTS: During a mean follow-up period of 41.6 months (range 7 to 104), immunosuppressive treatment with high dose prednisone resulted in stable remission in all except one patient, who experienced one relapse. In this patient, the addition of azathioprine to prednisone induced a persistent remission, which remained after 1-year follow-up. During treatment, three patients had severe steroid-related adverse effects that in two patients required replacement of prednisone with azathioprine and cyclophosphamide, respectively. This variation in the immunosuppressive regimen did not modify the favorable clinical outcome. CONCLUSIONS: The dose and duration of steroid treatment are critical factors in preventing recurrent pericarditis. High dose prednisone with aspirin should be considered in the treatment of recurrent pericarditis resistant to anti-inflammatory therapy. Cyclophosphamide or azathioprine should be reserved for patients who do not respond to high dose prednisone or who experience severe complications related to steroid therapy.

Adolescent↗
PubMed1995

CD8+ T lymphocytes in the lung of acquired immunodeficiency syndrome patients harbor human immunodeficiency virus type 1.

Human immunodeficiency virus-1 (HIV-1) infection of CD8+ lymphocytes has been described in several in vitro culture systems, but whether CD8+ cells are a target and also serve as a reservoir for infection in vivo as yet is unknown. We addressed this issue in patients with acquired immunodeficiency syndrome (AIDS)-related lower respiratory tract chronic inflammation, which is characterized by a massive influx of CD8+ HIV-1-specific cytotoxic T lymphocytes (CTL). Proviral load in lung T lymphocytes and their subpopulations was evaluated by using the DNA-polymerase chain reaction (PCR) technique on cells retrieved by bronchoalveolar lavage. To avoid the possibility that the presence of HIV-1 DNA could be caused by contaminating CD4+ cells, serial dilutions of highly purified CD8+ cells were also analyzed by PCR. Our findings showed that lung CD8+ cells harbor and express HIV-1. To explore the possible mechanisms leading to pulmonary CD8+ lymphocyte infection, we evaluated CD4 gene expression on highly purified CD8+ cells by means of reverse transcriptase PCR. Despite the lack of membrane CD4 reactivity, we could show that CD8+ cells may express CD4 RNA. Coinfection of lung CD8+ cells harboring proviral HIV-1 sequences by viral agents capable of inducing CD4 expression (ie, HHV-6) was not detected. Our data indicate that not only CD4+ T lymphocytes and macrophages, but also CD8+ cells, may represent a target and/or a reservoir for HIV-1 in vivo, and suggest that lung CD8+ lymphocytes could derive from precursors equipped with enough CD4 molecules to become HIV-1 permissive. Aside from the cell-to-cell contact between activated HIV-1 specific CTL and relevant targets, the infection of precursors could represent an additional mechanism accounting for the infection of pulmonary CD8+ cells and their functional impairment.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Expression of TNF receptors by T cells and membrane TNF-alpha by alveolar macrophages suggests a role for TNF-alpha in the regulation of the local immune responses in the lung of HIV-1-infected patients.

High amounts of TNF-alpha are released by alveolar macrophages (AMs) in the lungs of patients with HIV-1 infection. To investigate the role of this cytokine in the local immune response, we studied the expression of surface receptors for TNF-alpha (TNF-Rs) and the presence of the transmembrane form of TNF-alpha (mTNF-alpha) on bronchoalveolar lavage (BAL) cells recovered from 14 patients with HIV-1 infection. The role of TNF-alpha both in the events leading to the T cell alveolitis and as a mediator of cytotoxicity was also evaluated. TNF-R expression was determined by flow cytometry on BAL CD8 lymphocytes and AMs (i.e., the cells that account for the alveolitis in HIV-1 infection). We found that CD8 cells express the 75-kDa (CD120a) but not the 55-kDa (CD120a) TNF-Rs, whereas AMs were devoid of TNF-R expression. More than 90% of BAL T cells efficiently bound TNF-alpha; when T cells were tested for their proliferative capacity, an up-regulation of the IL-2-mediated proliferation by TNF-alpha was observed, suggesting that this cytokine may drive the in situ proliferation of CD120b+ T cells. As shown by flow cytometry analysis and immunoprecipitation with anti-TNF-alpha Ab, mTNF-alpha expression was observed on AMs but not on alveolar T cells. Fixed AMs showed high levels of killing against TNF-sensitive targets. Taken together, our data demonstrate the selective expression of TNF-Rs and mTNF-alpha on cells accumulating within the alveolar spaces of patients with HIV-1 infection, pointing to the compound role of TNF-alpha in the local immune responses.

Adult↗
PubMed1995

Alveolar macrophages as a cell source of cytokine hyperproduction in HIV-related interstitial lung disease.

Pulmonary macrophages play an important role in the pathogenesis of the acquired immunodeficiency syndrome (AIDS). They are known to be discrete target cells for human immunodeficiency virus (HIV), and compelling evidence is accumulating that alveolar macrophages (AMs) from HIV-infected patients behave as versatile secretory cells that, acting as antigen-presenting cells, release a great variety of cytokines. The secretory products of AMs, pivotal to their immune effects, may contribute to localized immune dysregulation as well as to primary lung damage and clinical disease. Pulmonary macrophages are also thought to facilitate retroviral spread by their direct infection, by presenting HIV antigens to uninfected T cells, and by secreting cytokines that transactivate HIV expression. This review briefly considers the events underlying the role of AMs in the pulmonary defense mechanisms against HIV and AIDS-related opportunistic infections. Following a brief overview of immune mechanisms taking place in the lungs of HIV-infected subjects, we describe the specific role of AMs in the immune mechanisms devoted to recognizing and removing HIV-infected cells and controlling the local growth of opportunists. The pathogenetic role envisaged for macrophages in lung damage are also reviewed in the context of the known biology of these cells. Finally, this review examines the relevance of the retroviral infection of AMs in terms of pathogenesis of the HIV-related interstitial lung disease.

Antigen-Presenting Cells↗
PubMed1995

Tumour-infiltrating lymphocytes bear the 75 kDa tumour necrosis factor receptor.

Tumour necrosis factor alpha (TNF-alpha) is a cytokine with a variety of immunological properties. The identification of two receptors for this molecule, i.e. the 75 kDa and the 55 kDa TNF receptors (TNF-R), recently clarified the mechanisms through which this cytokine provides its wide range of immunomodulatory activities. In this study we have investigated the expression and the functional properties of these receptors on tumour-infiltrating lymphocytes (TILs) recovered from 17 patients with solid cancers (melanoma, colorectal carcinoma and lung cancer). To this end, TIL lines and freshly isolated TILs were evaluated for (a) the expression and the functional role of TNF receptors following culture in the presence of interleukin 2 (IL-2) and (b) the production of TNF-alpha following culture with IL-2 and the role of this cytokine in IL-2-driven TIL proliferation. Flow cytometry analysis demonstrated that TILs bear the 75 kDa TNF-R. Moreover, TIL lines express detectable messages for TNF-alpha and release this cytokine. Functional in vitro studies have shown that anti-TNF-alpha, as well as anti-75 kDa TNF-R antibodies, are able to inhibit the IL-2-induced TIL proliferation. These data demonstrate that TILs are equipped with a fully functional TNF-R system and suggest a putative role for this receptor and its ligand in the activation and expression of TILs following immunotherapy with IL-2.

Antibodies, Monoclonal↗
PubMed1995

Childhood onset cyclic neutropenia: G-CSF therapy restores neutrophil count but does not influence superoxide anion and cytokine release by neutrophils.

In this paper we describe the case of a 16-year-old boy with childhood onset cyclic neutropenia (CN) with a 21 d cycle who was successfully treated with recombinant granulocyte-colony stimulating factor (G-CSF). Cyclic therapy with G-CSF (5 micrograms/kg/d s.c. for 1 week every 21 d) maintained peripheral neutrophil count above the normal range, reduced the incidence of severe infections and significantly improved the patient's performance status throughout an 18-month follow-up. Phenotypic analysis of circulating lymphocytes demonstrated that G-CSF treatment does not modify the phenotypic profile of circulating B, T and NK cell populations. Circulating neutrophils released normal amounts of cytokines (including IL-1 beta, IL-8, TNF alpha) and superoxide anion during G-CSF therapy.

Adolescent↗
PubMed1995

Leukemic cells in hairy cell leukemia and B cell chronic lymphocytic leukemia release soluble TNF receptors.

The two tumor necrosis factor receptors (TNF-Rs) exist in their soluble form in different biological fluids. In this study we investigated the concentrations of soluble tumor necrosis factor receptors (sTNF-Rs) in the culture supernatants of leukemic cells and in the serum obtained from 33 patients: 12 with hairy cell leukemia (HCL) and 21 with B cell chronic lymphocytic leukemia (B-CLL). In seven patients with HCL, sTNF-Rs were also evaluated following in vivo treatment with interferon-alpha (IFN-alpha). Purified leukemic cells from patients with HCL and B-CLL spontaneously released sTNF-R75 but not sTNF-R55. The levels of sTNF-R75 were higher in supernatants obtained from cultured hairy cells than from cultures of B-CLL cells. The shedding of sTNF-R75 was further increased both in HCL and B-CLL subjects by some B cell-related stimuli, including BCGF, PMA, SAC and was partially inhibited by IFN-alpha in patients with HCL. Sera from HCL patients presented increased levels of both sTNF-Rs with respect to normal controls. Treatment of HCL patients with IFN-alpha resulted in a decrease in serum levels of sTNF-Rs, particularly sTNF-R75. These findings suggest that leukemic cells account for the increased serum levels of sTNF-R75 observed in patients with HCL and B-CLL, but not for sTNF-R55.

Antigens, CD↗
PubMed1995

Serologic and molecular evidence for a possible pathogenetic role of viral infection in CD3-negative natural killer-type lymphoproliferative disease of granular lymphocytes.

We studied a series of 18 patients with CD3- lymphoproliferative disease of granular lymphocytes (LDGL) for evidence of chronic viral infection, including Epstein-Barr (EBV), hepatitis B (HBV), hepatitis C (HCV), human T lymphotropic virus (HTLV), and human immunodeficiency virus (HIV). Although all patients tested had serologic evidence for past infection with EBV, polymerase chain reaction (PCR) analysis of peripheral blood mononuclear cell (PBMC) DNA utilizing specific EBV primers demonstrated the presence of EBV-DNA in only six of 17 CD3- LDGL cases. A previous history of HBV infection, as defined by the presence of circulating IgG anti-HBc antibodies associated with either HBsAg positivity or negativity, was documented in seven cases; however, viral DNA was not detected in PBMC of these patients using PCR with specific HBV primers. Specific anti-HCV antibodies, confirmed by recombinant immunoblot assay, were detected in five CD3- LDGL patients; PCR analysis demonstrated the presence of viral RNA in PBMC of two of these cases. No patient had antibodies to HTLV-I/II or HIV-1/2. Five patients were infected by more than one virus (two with HBV and EBV and three with HBV and HCV). Our results provide serologic evidence for past viral infection in the large majority of CD3- NK-type LDGL patients. These data suggest that viral infection may have played a role early in disease pathogenesis and may no longer be necessary in sustaining GL proliferation in CD3- NK-type LDGL.

Antigens, Viral↗
PubMed1995

HIV-related interstitial lung disease.

The progressive breakdown of the cell-mediated immunity, which characterizes the natural history of HIV infection, invariably leads to the development of miscellaneous opportunistic infections or neoplasms involving a number of tissues, including the respiratory tract. In particular, given the extent and the severity of most infectious complications, it is not surprising that respiratory failure is a common finding in patients who have AIDS-related interstitial lung disease. Extensive knowledge of the sequence of events that starts with HIV infection of CD4+ cells and leads to the development of respiratory complications has been recently achieved. The present understanding of the pathogenesis of AIDS-related interstitial lung disease comes from the evaluation of cell populations retrieved from bronchoalveolar lavage fluid. In particular, the information gained from bronchoalveolar lavage studies led to the realization that HIV strains are present in the respiratory tract of HIV-seropositive subjects at all stages of infection. Furthermore, the characterization of bronchoalveolar lavage fluid cells proved to be central in evaluating the striking local immunologic reactions that can be detected in the lungs of these patients. Bronchoalveolar lavage studies have also demonstrated that local protective mechanisms may cause the shift toward accelerated progression to AIDS and the development of respiratory failure. This reviews briefly examines clinical aspects and cellular patterns of HIV infection in the respiratory tract. We will also consider data showing that HIV infection evokes an inflammatory response, initiated and sustained by cytotoxic T lymphocytes and macrophages and mediated by a number of cytokines that amplify host defenses as well as facilitate the spread of the retrovirus throughout the lower respiratory tract.

HIV Infections↗