IL-7 Prevents Both Caspase-Dependent and -Independent Pathways That Lead to the Spontaneous Apoptosis of i-IEL

Yada, Shinichiro; Nukina, Hideyuki; Kishihara, Kenji; Takamura, Noriaki; Yoshida, Hiroki; Inagaki–Ohara, Kyoko; Nomoto, Kikuo; Lin, Tiejun

doi:10.1006/cimm.2001.1765

Cited by 24 publications

(18 citation statements)

References 49 publications

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“…Moreover, we used longitudinal sections of villi to study IEL compared to the horizontal sections studied by Elson et al This allowed us to map the stained cells along the longitudinal villus axis, and our findings suggest that the decrease in IEL after CT challenge may be explained by an induced migration of CD8 ϩ cells from intraepithelial positions toward the villus core and possibly also out of the villus with the afferent lymph. Further, very few lymphocytes were stained for active caspase-3, an effector molecule known to be important in the apoptosis of T cells, including, as confirmed by us in the present study, CD8 ϩ rat lymphocytes (11,32,42), at either of the time points examined, and no difference could be detected compared to the control. In addition, the microarray data did not show any increase in the level of Fas ligand, a gene that has been shown to become activated in many forms of T-cell apoptosis (31), after CT challenge.…”

Section: Discussionsupporting

confidence: 78%

Cholera Toxin Induces a Transient Depletion of CD8⁺Intraepithelial Lymphocytes in the Rat Small Intestine as Detected by Microarray and Immunohistochemistry

Flach¹,

Lange²,

Jennische

et al. 2005

Infect Immun

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Section: Discussionsupporting

confidence: 78%

Cholera Toxin Induces a Transient Depletion of CD8⁺Intraepithelial Lymphocytes in the Rat Small Intestine as Detected by Microarray and Immunohistochemistry

Flach¹,

Lange²,

Jennische

et al. 2005

Infect Immun

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“…It is reasonable to assume that the mechanisms responsible for ischemia-reperfusioninduced apoptosis in intestinal epithelial cells may also directly induce apoptosis of lymphocytes. A loss of intestinal epithelial cells via apoptosis after ischemia-reperfusion could indirectly induce intestinal lymphocyte apoptosis though growth factor withdrawal because cytokines such as IL-7 and IL-15 are produced by intestinal epithelial cells (23,36) and these cytokines provide essential survival signals as well as prevent apoptosis of intraepithelial lymphocytes (50). Whether the loss of intestinal lymphocytes represents a direct effect of ischemia and reperfusion on intestinal lymphocytes or an indirect effect due to cytokine withdrawal as a result of atrophy of epithelial cells remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

Adrenalectomy in mice does not prevent loss of intestinal lymphocytes after exercise

Hoffman‐Goetz

Quadrilatero

Boudreau

et al. 2004

Journal of Applied Physiology

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Exhaustive exercise is associated with an increase in circulating glucocorticoids (GCs), lymphocyte apoptosis, and a reduction in intestinal lymphocyte number. The present study examined the role of GCs on the numerical changes seen in intestinal lymphocytes after exercise. Female C57BL/6 mice were bilaterally adrenalectomized (ADX; n ϭ 18) or given sham surgery (Sham; n ϭ 18) and assigned to one of three exercise conditions: treadmill running (28 m/min, 90 min, 2°slope) and killed immediately or after 24 h recovery, or not exercised and killed immediately after 90-min exposure to the treadmill environment. Lymphocytes were isolated from the intestines with CD45 ϩ cells collected by positive selection using magnetic bead separation columns, and lymphocyte subpopulations were analyzed by flow cytometry for CD45 ϩ , CD3␣␤ ϩ , CD3␥␦ ϩ , CD8␤ ϩ , CD8␣ ϩ , CD4 ϩ , and NK ϩ phenotypic markers. ADX mice had significantly more intestinal CD45 ϩ leukocytes (P Ͻ 0.05) and CD3␣␤ ϩ (P Ͻ 0.05), CD3␥␦ ϩ (P Ͻ 0.01), CD8␣ ϩ (P Ͻ 0.001), and NK ϩ (P Ͻ 0.05) intestinal lymphocytes than Sham mice. There was a significant effect of exercise condition on total intestinal CD45 ϩ leukocytes (P Ͻ 0.01) and CD3␣␤ ϩ (P Ͻ 0.05), CD8␣ ϩ (P Ͻ 0.001), and CD4 ϩ (P Ͻ 0.05) intestinal lymphocytes, with fewer cells at 24 h postexercise compared with the other treatment conditions. There were no surgical ϫ exercise interaction effects on the CD3 and CD8 phenotype numbers. Plasma corticosterone was virtually nil in ADX mice regardless of exercise condition but was significantly elevated in Sham mice immediately postexercise (P Ͻ 0.001). The data indicate that ADX does not prevent the loss of lymphocytes from the intestinal mucosa 24 h after strenuous exercise and GCs are not directly causal in the leukopenia of exercise. treadmill running; adrenal glands; glucocorticoids NUMEROUS STUDIES HAVE SHOWN that acute exercise is associated with induction of apoptosis or programmed cell death and loss of lymphocytes from blood, thymus, and spleen in humans and laboratory animals (9,20,28,29). Lymphocyte loss and/or apoptosis have been observed in other situations characterized by extreme physiological stress, including burn injury (15), electrical shock (48), and chronic restraint stress (42), and may reflect release of stress hormones, in particular glucocorticoids (GCs). GCs trigger apoptosis in lymphocytes by acting on an intracellular pathway via the mitochondria (2), which results in the accumulation of mitochondrial derived cytochrome c within the cytosol, loss of mitochondrial membrane integrity, externalization of phosphatidylserine at cell membranes, and DNA fragmentation (27,45).The intestinal intraepithelial lymphocytes (IELs) are a unique population of T cells that function as a first line of defense against exogenous pathogens, many of which develop independently of the thymus gland [i.e., T cells with the ␥␦ form of the T cell receptor (TCR)] (35). IELs play an important role in protection from epithelial tumor cells through their function a...

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“…Fourth, the mammalian intestine can promote the differentiation of T cell precursors from bone marrow progenitors [6][7][8], and the intestine appears to provide both contactmediated and humoral components necessary for the maturation of T cells [9]. Consistent with that, developing IELs have receptors for IL-7 and use IL-7 for survival and maturation [10,11].…”

Section: Introductionmentioning

confidence: 99%

Intestinal TSH production is localized in crypt enterocytes and in villus ‘hotblocks’ and is coupled to IL-7 production: evidence for involvement of TSH during acute enteric virus infection

et al. 2005

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The immune and neuroendocrine systems have been shown to work conjointly in a number of ways. One aspect of this has to do with a potential role for thyroid stimulating hormone (TSH) in the regulation of the mucosal immune system, although the mechanisms by which this occurs remain vague. To more thoroughly understand how TSH participates in intestinal intraepithelial lymphocyte (IEL) development and immunity, experiments have been conducted to define local sites of intestinal TSH production, and to characterize changes that occur in the synthesis of TSH during acute enteric virus infection. Here, we demonstrate that TSH in the small intestine is specifically localized to regions below villus crypts as seen by immunocytochemical staining, which revealed high-level TSH staining in lower crypts in the absence of IL-7 staining, and TSH and IL-7 costaining in upper crypt regions. Additionally, prominent TSH staining was evident in TSH 'hotblocks' sparsely dispersed throughout the epithelial layer. In rotavirus-infected mice, the TSH staining pattern differed significantly from that of non-infected animals. Notably, at 2 and 3 days post-infection, TSH expression was high in and near apical villi where virus infection was greatest. These findings lend credence to the notion that TSH plays a role both in the development of intestinal T cells, and in the process of local immunity during enteric virus infection.

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IL-7 Prevents Both Caspase-Dependent and -Independent Pathways That Lead to the Spontaneous Apoptosis of i-IEL

Cited by 24 publications

References 49 publications

Cholera Toxin Induces a Transient Depletion of CD8⁺Intraepithelial Lymphocytes in the Rat Small Intestine as Detected by Microarray and Immunohistochemistry

Cholera Toxin Induces a Transient Depletion of CD8⁺Intraepithelial Lymphocytes in the Rat Small Intestine as Detected by Microarray and Immunohistochemistry

Adrenalectomy in mice does not prevent loss of intestinal lymphocytes after exercise

Intestinal TSH production is localized in crypt enterocytes and in villus ‘hotblocks’ and is coupled to IL-7 production: evidence for involvement of TSH during acute enteric virus infection

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IL-7 Prevents Both Caspase-Dependent and -Independent Pathways That Lead to the Spontaneous Apoptosis of i-IEL

Cited by 24 publications

References 49 publications

Cholera Toxin Induces a Transient Depletion of CD8+Intraepithelial Lymphocytes in the Rat Small Intestine as Detected by Microarray and Immunohistochemistry

Cholera Toxin Induces a Transient Depletion of CD8+Intraepithelial Lymphocytes in the Rat Small Intestine as Detected by Microarray and Immunohistochemistry

Adrenalectomy in mice does not prevent loss of intestinal lymphocytes after exercise

Intestinal TSH production is localized in crypt enterocytes and in villus ‘hotblocks’ and is coupled to IL-7 production: evidence for involvement of TSH during acute enteric virus infection

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Cholera Toxin Induces a Transient Depletion of CD8⁺Intraepithelial Lymphocytes in the Rat Small Intestine as Detected by Microarray and Immunohistochemistry

Cholera Toxin Induces a Transient Depletion of CD8⁺Intraepithelial Lymphocytes in the Rat Small Intestine as Detected by Microarray and Immunohistochemistry