The Experts below are selected from a list of 318 Experts worldwide ranked by ideXlab platform
Jörg Reimann - One of the best experts on this subject based on the ideXlab platform.
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commensal gut flora drives the expansion of proinflammatory cd4 t cells in the Colonic Lamina Propria under normal and inflammatory conditions
Journal of Immunology, 2008Co-Authors: Jan Hendrik Niess, Frank Leithauser, Guido Adler, Jörg ReimannAbstract:We tested in B6 mice whether the local expansion of CD4 T cells producing proinflammatory cytokines including IL-17 (Th17 cells) in the Colonic Lamina Propria (cLP) depends on the commensal microflora. High numbers of CD4 Th17 cells were found in the Lamina Propria of the ileum and colon but not the duodenum, jejunum, mesenteric lymph nodes, spleen, or liver of specific pathogen-free (SPF) mice. The microflora is required for the accumulation of cytokine (IL-17, IFN-γ, TNF-α, IL-10)-producing CD4 T cells in the cLP because only low numbers of cytokine-producing cLP CD4 T cells were found in syngeneic (age- and sex-matched) germfree mice. The fraction of cLP Th17 cells was higher in (type I and type II) IFN- but not IL-4- or IL-12p40-deficient SPF congenics. cLP CD4 Th17 cells produce IL-17 but not IFN-γ, TNF-α, IL-4, or IL-10. cLP CD4 Th17 cells accumulate locally in colitis induced by adoptive transfer of IFN-γ+/+ or IFN-γ−/− CD4 T cells into congenic SPF (but not germfree) RAG−/− hosts. In this colitis model, cLP CD4 T cells that “spontaneously” produce IL-17 progressively increase in number in the inflamed cLP, and increasing serum IL-17 levels appear as the disease progresses. Commensal bacteria-driven, local expansion of cLP CD4 Th17 cells may contribute to the pathogenesis of this inflammatory bowel disease.
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Colitis-Inducing Potency of CD4+ T Cells in Immunodeficient, Adoptive Hosts Depends on Their State of Activation, IL-12 Responsiveness, and CD45RB Surface Phenotype
Journal of immunology (Baltimore Md. : 1950), 1999Co-Authors: Mogens H. Claesson, Kerstin Bonhagen, Frank Leithauser, Peter Moller, Søren Bregenholt, Stefan Thoma, Michael J. Grusby, Mogens Holst Nissen, Jörg ReimannAbstract:We studied the induction, severity, and rate of progression of inflammatory bowel disease (IBD) induced in SCID mice by the adoptive transfer of low numbers of the following purified BALB/c CD4 + T cell subsets: 1) unfractionated, peripheral, small (resting), or large (activated) CD4 + T cells; 2) fractionated, peripheral, small, or large, CD45RB high or CD45RB low CD4 + T cells; and 3) peripheral IL-12-unresponsive CD4 + T cells from STAT-4-deficient mice. The adoptive transfer into SCID host of comparable numbers of CD4 + T cells was used to assess the colitis-inducing potency of these subsets. Small CD45RB high CD4 + T lymphocytes and activated CD4 + T blasts induced early (6–12 wk posttransfer) and severe disease, while small resting and unfractionated CD4 + T cells or CD45RB low T lymphocytes induced a late-onset disease 12–16 wk posttransfer. SCID mice transplanted with STAT-4 −/− CD4 + T cells showed a late-onset IBD manifest >20 wk posttransfer. In SCID mice with IBD transplanted with IL-12-responsive CD4 + T cells, the Colonic Lamina Propria CD4 + T cells showed a mucosa-seeking memory/effector CD45RB low Th1 phenotype abundantly producing IFN-γ and TNF-α. In SCID mice transplanted with IL-12-unresponsive STAT-4 −/− CD4 + T cells, the Colonic Lamina Propria, mesenteric lymph node, and splenic CD4 + T cells produced very little IFN-γ but abundant levels of TNF-α. The histopathologic appearance of colitis in all transplanted SCID mice was similar. These data indicate that CD45RB high and CD45RB low , IL-12-responsive and IL-12-unresponsive CD4 + T lymphocytes and lymphoblasts have IBD-inducing potential though of varying potency.
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A pancolitis resembling human ulcerative colitis (UC) is induced by CD4+ TCR alphabeta T cells of athymic origin in histocompatible severe combined immunodeficient (SCID) mice.
Clinical and experimental immunology, 1998Co-Authors: Kerstin Bonhagen, S. Thoma, Leithäuser F, Möller P, Jörg ReimannAbstract:CD4+ TCRalphabeta+ T cells from the Colonic Lamina Propria of athymic (nude) mice were adoptively transferred into histocompatible (SCID) mice homozygous for the autosomal recessive mutation scid (severe combined immunodeficiency). Transfer of these extrathymic CD4+ T cells into SCID mice induced a pancolitis in the adoptive host. The histopathology of this inflammatory response was restricted to the colon and closely resembled human UC. CD4+ T cells infiltrating the Colonic Lamina Propria of diseased SCID mice displayed the surface phenotype of mucosa-seeking memory/effector cells, expressed interferon-gamma (IFN-gamma), and lysed targets in a Fas (CD95)/FasL-dependent pathway. Massive accumulation of oligoclonal CD4+ T cells of athymic origin with the phenotype of Th1 memory/effector T cells in the Colonic Lamina Propria of a histocompatible, immunodeficient host elicits a pancolitis that morphologically mimics human UC.
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Polyclonal expansion of adoptively transferred CD4+ αβ T cells in the Colonic Lamina Propria of scid mice with colitis
European Journal of Immunology, 1996Co-Authors: Angelika Rudolphi, Kerstin Bonhagen, Jörg ReimannAbstract:The adoptive transfer of low numbers of peripheral, non-fractionated CD4+ alpha beta T cells into histocompatible, severely immunodeficient (scid) hosts induces a colitis. This disease developed in C.B-17 scid/scid hosts after the injection of 10(5) CD4+ T cells purified from different peripheral lymphoid organs of immunocompetent C.B.-17 +/+ or BALB/cdm2 donor mice. Irrespective of their tissue origin, transferred CD4+ T cells selectively repopulated the scid host with gut-seeking CD4+ T cells. A chronic inflammatory bowel disease (IBD) developed as polyclonal populations of mucosa-seeking memory/effector CD4+ T cells accumulated in the gut Lamina Propria and epithelial layer of the adoptive host. The manifestation of colitis in the scid host correlated with the in situ polyclonal activation and expansion of adoptively transferred CD4+ T cells in the Colonic Lamina Propria. Attempts were unsuccessful to select in vivo an oligoclonal CD4+ T cell population with an enhanced IBD-inducing potential by repeatedly reinjecting 10(5) donor-type CD4+ T cells from the Colonic Lamina Propria of transplanted scid mice with an early and severe IBD into new scid hosts. The data indicate that the preferential repopulation of gut-associated lymphoid tissues with immunocompetent CD4+ T cells, and their polyclonal activation and in situ expansion in the Lamina Propria of the histocompatible, immunodeficient host are critical events in the pathogenesis of an IBD in this model.
Richard P Macdermott - One of the best experts on this subject based on the ideXlab platform.
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mice with a selective deletion of the cc chemokine receptors 5 or 2 are protected from dextran sodium sulfate mediated colitis lack of cc chemokine receptor 5 expression results in a nk1 1 lymphocyte associated th2 type immune response in the intesti
Journal of Immunology, 2000Co-Authors: Pietro G Andres, Paul L Beck, Atul K Bhan, Tracey C Dawson, Atsushi Mizoguchi, Emiko Mizoguchi, William A Kuziel, Richard P Macdermott, Nobuyo MaedaAbstract:The chemokine receptors CCR2 and CCR5 and their respective ligands regulate leukocyte chemotaxis and activation. To determine the role of these chemokine receptors in the regulation of the intestinal immune response, we induced colitis in CCR2- and CCR5-deficient mice by continuous oral administration of dextran sodium sulfate (DSS). Both CCR2- and CCR5-deficient mice were susceptible to DSS-induced intestinal inflammation. The lack of CCR2 or CCR5 did not reduce the DSS-induced migration of macrophages into the Colonic Lamina Propria. However, both CCR5-deficient mice and, to a lesser degree, CCR2-deficient mice were protected from DSS-induced intestinal adhesions and mucosal ulcerations. CCR5-deficient mice were characterized by a greater relative infiltration of CD4+ and NK1.1+ lymphocyte in the Colonic Lamina Propria when compared to wild-type and CCR2-deficient mice. In CCR5-deficient mice, mucosal mRNA expression of IL-4, IL-5, and IL-10 was increased, whereas that of IFN-γ was decreased, corresponding to a Th2 pattern of T cell activation. In CCR2-deficient mice, the infiltration of Th2-type T cells in the Lamina Propria was absent, but increased levels of IL-10 and decreased levels of IFN-γ may have down regulated mucosal inflammation. Our data indicate that CCR5 may be critical for the promotion of intestinal Th1-type immune responses in mice.
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Increased in vitro release of soluble interleukin 2 receptor by Colonic Lamina Propria mononuclear cells in inflammatory bowel disease.
Gut, 1992Co-Authors: Stefan Schreiber, Andreas Raedler, A R Conn, J L Rombeau, Richard P MacdermottAbstract:Increased concentrations of the soluble form of the interleukin 2 receptor have been observed in the sera of Crohn's disease and ulcerative colitis patients. In this study we have observed the spontaneous release of soluble interleukin 2 receptor by unstimulated, isolated normal and inflammatory bowel disease Colonic Lamina Propria mononuclear cells. Lamina Propria mononuclear cells from Crohn's disease patients (median = 204 U/ml (interquartile range 126-396, n 17) secreted significantly (p less than 0.01) more soluble interleukin 2 receptor than normal controls (median = 124.5 U/ml (108-131), n 12). No statistically significant differences were seen between ulcerative colitis (median = 135 U/ml (92-196), n 20) and normal controls. Moreover, significantly (p less than 0.01) increased amounts of soluble interleukin 2 receptor were secreted by Colonic diverticulitis Lamina Propria mononuclear cells (median = 259 U/ml (149-282), n 15) which were used as disease specificity controls. Time course experiments showed that the majority of soluble interleukin 2 receptor was released by isolated Lamina Propria mononuclear cells in the first six days of culture. Upon stimulation with pokeweed mitogen, Crohn's disease (median = 2258 U/ml (1435-3584), n 14), normal control (median = 2622 U/ml (2030-3180), n 14) and diverticulitis Lamina Propria mononuclear cells (median = 2745 U/ml (1733-3192), n 10) reached similar maximal soluble interleukin 2 receptor secretion levels, while ulcerative colitis Lamina Propria mononuclear cells secreted significantly (p less than 0.005) less soluble interleukin 2 receptor (median = 912 U/ml (494-1259), n 17). These results suggest that enhanced shedding/secretion of soluble interleukin 2 receptor by intestinal lymphocytes may account in part for increased serum soluble interleukin 2 receptor concentrations during chronic intestinal inflammatory reactions.
Xiaohui Zhao - One of the best experts on this subject based on the ideXlab platform.
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Multinucleated stromal giant cells in Colonic Lamina Propria
Histopathology, 2007Co-Authors: Xiaohui ZhaoAbstract:Aims: Multinucleated stromal giant cells occur in the anus, genitals and many other organs. They resemble myofibroblasts, react to local injury and are found incidentally or in association with various lesions. They have only rarely been reported to occur in the colon. The aim was to firmly establish their existence in colorectal Lamina Propria. Methods and results: Specimens from one hundred biopsies taken from throughout the colon (70%) and rectum (30%) were retrospectively reviewed. Multinucleated stromal giant cells occurred in 23 specimens (23%), were panColonic but surprisingly spared rectal mucosa (0%). Multinucleated stromal giant cells occurred in both normal mucosa and abnormal mucosa and appeared to be larger and more numerous in abnormal mucosa than in normal mucosa. Specimens with tubular adenomas appeared to have strikingly abundant multinucleated stromal giant cells with large numbers of nuclei. Immunohistochemistry and ultrastructural examination showed features consistent with myofibroblastic differentiation. Conclusions: We have firmly established the existence of multinucleated stromal giant cells in Colonic Lamina Propria and confirm their myofibroblastic differentiation. They may be more common in abnormal mucosa and particularly prominent in the setting of tubular adenoma. Absence of rectal multinucleated stromal giant cells may represent a microanatomical difference between the colon and rectum.
Kerstin Bonhagen - One of the best experts on this subject based on the ideXlab platform.
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Colitis-Inducing Potency of CD4+ T Cells in Immunodeficient, Adoptive Hosts Depends on Their State of Activation, IL-12 Responsiveness, and CD45RB Surface Phenotype
Journal of immunology (Baltimore Md. : 1950), 1999Co-Authors: Mogens H. Claesson, Kerstin Bonhagen, Frank Leithauser, Peter Moller, Søren Bregenholt, Stefan Thoma, Michael J. Grusby, Mogens Holst Nissen, Jörg ReimannAbstract:We studied the induction, severity, and rate of progression of inflammatory bowel disease (IBD) induced in SCID mice by the adoptive transfer of low numbers of the following purified BALB/c CD4 + T cell subsets: 1) unfractionated, peripheral, small (resting), or large (activated) CD4 + T cells; 2) fractionated, peripheral, small, or large, CD45RB high or CD45RB low CD4 + T cells; and 3) peripheral IL-12-unresponsive CD4 + T cells from STAT-4-deficient mice. The adoptive transfer into SCID host of comparable numbers of CD4 + T cells was used to assess the colitis-inducing potency of these subsets. Small CD45RB high CD4 + T lymphocytes and activated CD4 + T blasts induced early (6–12 wk posttransfer) and severe disease, while small resting and unfractionated CD4 + T cells or CD45RB low T lymphocytes induced a late-onset disease 12–16 wk posttransfer. SCID mice transplanted with STAT-4 −/− CD4 + T cells showed a late-onset IBD manifest >20 wk posttransfer. In SCID mice with IBD transplanted with IL-12-responsive CD4 + T cells, the Colonic Lamina Propria CD4 + T cells showed a mucosa-seeking memory/effector CD45RB low Th1 phenotype abundantly producing IFN-γ and TNF-α. In SCID mice transplanted with IL-12-unresponsive STAT-4 −/− CD4 + T cells, the Colonic Lamina Propria, mesenteric lymph node, and splenic CD4 + T cells produced very little IFN-γ but abundant levels of TNF-α. The histopathologic appearance of colitis in all transplanted SCID mice was similar. These data indicate that CD45RB high and CD45RB low , IL-12-responsive and IL-12-unresponsive CD4 + T lymphocytes and lymphoblasts have IBD-inducing potential though of varying potency.
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A pancolitis resembling human ulcerative colitis (UC) is induced by CD4+ TCR alphabeta T cells of athymic origin in histocompatible severe combined immunodeficient (SCID) mice.
Clinical and experimental immunology, 1998Co-Authors: Kerstin Bonhagen, S. Thoma, Leithäuser F, Möller P, Jörg ReimannAbstract:CD4+ TCRalphabeta+ T cells from the Colonic Lamina Propria of athymic (nude) mice were adoptively transferred into histocompatible (SCID) mice homozygous for the autosomal recessive mutation scid (severe combined immunodeficiency). Transfer of these extrathymic CD4+ T cells into SCID mice induced a pancolitis in the adoptive host. The histopathology of this inflammatory response was restricted to the colon and closely resembled human UC. CD4+ T cells infiltrating the Colonic Lamina Propria of diseased SCID mice displayed the surface phenotype of mucosa-seeking memory/effector cells, expressed interferon-gamma (IFN-gamma), and lysed targets in a Fas (CD95)/FasL-dependent pathway. Massive accumulation of oligoclonal CD4+ T cells of athymic origin with the phenotype of Th1 memory/effector T cells in the Colonic Lamina Propria of a histocompatible, immunodeficient host elicits a pancolitis that morphologically mimics human UC.
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Polyclonal expansion of adoptively transferred CD4+ αβ T cells in the Colonic Lamina Propria of scid mice with colitis
European Journal of Immunology, 1996Co-Authors: Angelika Rudolphi, Kerstin Bonhagen, Jörg ReimannAbstract:The adoptive transfer of low numbers of peripheral, non-fractionated CD4+ alpha beta T cells into histocompatible, severely immunodeficient (scid) hosts induces a colitis. This disease developed in C.B-17 scid/scid hosts after the injection of 10(5) CD4+ T cells purified from different peripheral lymphoid organs of immunocompetent C.B.-17 +/+ or BALB/cdm2 donor mice. Irrespective of their tissue origin, transferred CD4+ T cells selectively repopulated the scid host with gut-seeking CD4+ T cells. A chronic inflammatory bowel disease (IBD) developed as polyclonal populations of mucosa-seeking memory/effector CD4+ T cells accumulated in the gut Lamina Propria and epithelial layer of the adoptive host. The manifestation of colitis in the scid host correlated with the in situ polyclonal activation and expansion of adoptively transferred CD4+ T cells in the Colonic Lamina Propria. Attempts were unsuccessful to select in vivo an oligoclonal CD4+ T cell population with an enhanced IBD-inducing potential by repeatedly reinjecting 10(5) donor-type CD4+ T cells from the Colonic Lamina Propria of transplanted scid mice with an early and severe IBD into new scid hosts. The data indicate that the preferential repopulation of gut-associated lymphoid tissues with immunocompetent CD4+ T cells, and their polyclonal activation and in situ expansion in the Lamina Propria of the histocompatible, immunodeficient host are critical events in the pathogenesis of an IBD in this model.
Martin R. Goodier - One of the best experts on this subject based on the ideXlab platform.
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increased proportion of cd16 nk cells in the Colonic Lamina Propria of inflammatory bowel disease patients but not after azathioprine treatment
Alimentary Pharmacology & Therapeutics, 2011Co-Authors: Alan Steel, Christopher M. Mela, James O. Lindsay, B Gazzard, Martin R. GoodierAbstract:BACKGROUND: Distinct functional subsets of natural killer cells potentially contribute to the pathology of inflammatory bowel disease (IBD). AIM: To report the phenotypic and functional characteristics of natural killer cells in blood and Lamina Propria of IBD patients, and the effect of azathioprine. METHODS: Natural killer cells from blood and Lamina Propria of healthy controls or patients with Crohn's disease, or ulcerative colitis were studied by flow cytometry. Activation, cytokine production, proliferation and apoptosis of natural killer cell subsets were studied in vitro. RESULTS: CD16(+) natural killer cells are increased in frequency in the Lamina Propria comparing Crohn's disease or ulcerative colitis with healthy controls. Azathioprine therapy was associated with a reduction in total natural killer cells in blood and Lamina Propria, preferentially of the CD16(+) subset. Azathioprine therapy did not impair natural killer degranulation, but reduced natural and cytokine-activated cytotoxicity and interferon-gamma (IFN-γ) production. Culture of resting peripheral blood mononuclear cells with azathioprine resulted in loss of natural killer cells and inhibition of activation and IFN-γ production. Azathioprine preferentially inhibited proliferation of CD16(+) natural killer cells and induced apoptosis in resting but not in pre-activated natural killer cells. CONCLUSIONS: Natural killer cells with cytolytic potential are enriched in the Colonic Lamina Propria of individuals with IBD. Azathioprine is associated with a reduction in these cells and a normalization of natural killer cell populations.
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increased proportion of cd16 nk cells in the Colonic Lamina Propria of inflammatory bowel disease patients but not after azathioprine treatment
Alimentary Pharmacology & Therapeutics, 2011Co-Authors: Alan Steel, Christopher M. Mela, James O. Lindsay, B Gazzard, Martin R. GoodierAbstract:Aliment Pharmacol Ther 2011; 33: 115–126 Summary Background Distinct functional subsets of natural killer cells potentially contribute to the pathology of inflammatory bowel disease (IBD). Aim To report the phenotypic and functional characteristics of natural killer cells in blood and Lamina Propria of IBD patients, and the effect of azathioprine. Methods Natural killer cells from blood and Lamina Propria of healthy controls or patients with Crohn’s disease, or ulcerative colitis were studied by flow cytometry. Activation, cytokine production, proliferation and apoptosis of natural killer cell subsets were studied in vitro. Results CD16+ natural killer cells are increased in frequency in the Lamina Propria comparing Crohn’s disease or ulcerative colitis with healthy controls. Azathioprine therapy was associated with a reduction in total natural killer cells in blood and Lamina Propria, preferentially of the CD16+ subset. Azathioprine therapy did not impair natural killer degranulation, but reduced natural and cytokine-activated cytotoxicity and interferon-gamma (IFN-γ) production. Culture of resting peripheral blood mononuclear cells with azathioprine resulted in loss of natural killer cells and inhibition of activation and IFN-γ production. Azathioprine preferentially inhibited proliferation of CD16+ natural killer cells and induced apoptosis in resting but not in pre-activated natural killer cells. Conclusions Natural killer cells with cytolytic potential are enriched in the Colonic Lamina Propria of individuals with IBD. Azathioprine is associated with a reduction in these cells and a normalization of natural killer cell populations.
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Increased proportion of CD16(+) NK cells in the Colonic Lamina Propria of inflammatory bowel disease patients, but not after azathioprine treatment.
Alimentary Pharmacology & Therapeutics, 2010Co-Authors: Alan Steel, Christopher M. Mela, James O. Lindsay, B Gazzard, Martin R. GoodierAbstract:Aliment Pharmacol Ther 2011; 33: 115–126 Summary Background Distinct functional subsets of natural killer cells potentially contribute to the pathology of inflammatory bowel disease (IBD). Aim To report the phenotypic and functional characteristics of natural killer cells in blood and Lamina Propria of IBD patients, and the effect of azathioprine. Methods Natural killer cells from blood and Lamina Propria of healthy controls or patients with Crohn’s disease, or ulcerative colitis were studied by flow cytometry. Activation, cytokine production, proliferation and apoptosis of natural killer cell subsets were studied in vitro. Results CD16+ natural killer cells are increased in frequency in the Lamina Propria comparing Crohn’s disease or ulcerative colitis with healthy controls. Azathioprine therapy was associated with a reduction in total natural killer cells in blood and Lamina Propria, preferentially of the CD16+ subset. Azathioprine therapy did not impair natural killer degranulation, but reduced natural and cytokine-activated cytotoxicity and interferon-gamma (IFN-γ) production. Culture of resting peripheral blood mononuclear cells with azathioprine resulted in loss of natural killer cells and inhibition of activation and IFN-γ production. Azathioprine preferentially inhibited proliferation of CD16+ natural killer cells and induced apoptosis in resting but not in pre-activated natural killer cells. Conclusions Natural killer cells with cytolytic potential are enriched in the Colonic Lamina Propria of individuals with IBD. Azathioprine is associated with a reduction in these cells and a normalization of natural killer cell populations.
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Increased proportion of CD16+ NK cells in the Colonic Lamina Propria of IBD patients but not after Azathioprine treatment.
Alimentary Pharmacology and Therapeutics, 2010Co-Authors: Alan W Steel, Christopher M. Mela, B Gazzard, James Oliver Lindsay, Martin R. GoodierAbstract:Background: Distinct functional subsets of natural killer(NK) cells potentially contribute to the pathology of inflammatory bowel diseases(IBD). Aim: To report the phenotypic and functional characteristics of NK cells in blood and Lamina Propria(LP) of IBD patients, and the effect of azathioprine. Methods: NK cells from blood and LP of healthy controls(HC) or patients with Crohn's disease(CD), or ulcerative colitis(UC) were studied by flow cytometry. Activation, cytokine production, proliferation and apoptosis of NK cell subsets were studied in-vitro. Results: CD16+NK cells are increased in frequency in the LP comparing CD or UC with HC. Azathioprine therapy was associated with a reduction of total NK cells in blood and LP, preferentially of the CD16+ subset. Azathioprine therapy did not impair NK degranulation, but reduced natural and cytokine activated cytotoxicity and interferon-gamma(IFN-γ production. Culture of resting PBMC with azathioprine resulted in loss of NK cells and inhibition of activation and IFN-γ production. Azathioprine preferentially inhibited proliferation of CD16+ NK cells and induced apoptosis in resting but not in pre-activated NK cells. Conclusions: NK cells with cytolytic potential are enriched in the Colonic LP of individuals with IBD. Azathioprine is associated with a reduction in these cells and a normalisation of NK cell populations.
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Depletion of natural killer cells in the Colonic Lamina Propria of viraemic HIV-1-infected individuals.
AIDS, 2007Co-Authors: Christopher M. Mela, Alan Steel, James O. Lindsay, Brian Gazzard, Frances Gotch, Martin R. GoodierAbstract:BACKGROUND HIV-1 infection is known to have a detrimental impact on peripheral blood natural killer cell phenotype and function. Chronic HIV-1 also causes a substantial depletion of CD4+ T cells in the gastrointestinal tract and the blood. OBJECTIVE To investigate the impact of chronic HIV-1 infection with on natural killer cell populations in the gastrointestinal tract and the effect of suppression of plasma viraemia with antiretroviral therapy. METHODS Lymphocyte populations were extracted from the Lamina Propria of biopsies taken from the sigmoid colon of HIV-1-infected and uninfected individuals. The proportions of natural killer cell subsets were compared in viraemic (n = 15) and aviraemic HIV-1-positive, HAART-treated individuals (n = 27) and HIV-1 negative control individuals (n = 26) using flow cytometry on gated subsets. RESULTS Natural killer cells are depleted in Colonic biopsies from HIV-1-infected individuals with detectable plasma virus in comparison with HIV-1-negative individuals. A significant increase in the proportion of both natural killer and CD4+ T cells in the Colonic Lamina Propria is observed in aviraemic individuals compared to viraemic individuals. CONCLUSIONS Chronic HIV-1 infection results in depletion of both natural killer cells and CD4+ T cells in Colonic tissue and antiretroviral therapy results in a recovery of these subsets in individuals with undetectable plasma viral load.