Expression of mucosal homing receptor alpha4beta7 by circulating CD4+ cells with memory for intestinal rotavirus.

Rott, Lusijah S.; Rose, Jim; Bass, Dorsey; Williams, Marna; Greenberg, Harry B.; Butcher, Eugene C.

doi:10.1172/jci119633

Cited by 137 publications

(112 citation statements)

References 21 publications

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“…ear injection of CPE evoked late-phase cutaneous responses, as demonstrated by ear thickness with a concomitant influx of eosinophils into the ear tissue. The current understanding is that the initial site of Ag priming, i.e., the draining LNs, where dendritic cells (DCs) carrying Ag first interact with T cells, determines the future homing of memory/effector T cells and, hence, the site at which immune-inflammatory responses will manifest upon Ag re-exposure (23)(24)(25)(26)(27). This notion along with the observations that we made in the lung and skin prompted us to comprehensively seek for evidence of peanut-specific immunity in a variety of LNs.…”

Section: Discussionmentioning

confidence: 99%

Impact of CD40 Ligand, B Cells, and Mast Cells in Peanut-Induced Anaphylactic Responses

Sun

Arias

Álvarez

et al. 2007

The Journal of Immunology

106

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The effector immune mechanisms underlying peanut-induced anaphylaxis remain to be fully elucidated. We investigated the relative contribution of Igs, mast cells (MCs), and FcεRI in the elicitation of anaphylaxis in a murine model. Assessment of peanut hypersensitivity reactions was performed clinically and biologically. Our data show that wild-type (WT; C57BL/6 strain) mice consistently developed severe anaphylaxis (median clinical score: 3.5/5), an ∼8°C drop in core body temperature, and significantly increased plasma levels of histamine and leukotrienes. CD40 ligand- and B cell-deficient mice presented evidence of allergic sensitization as demonstrated by production of Th2-associated cytokines by splenocytes and a late-phase inflammatory response that were both indistinguishable to those detected in WT mice. However, CD40 ligand- and B cell-deficient mice did not exhibit any evidence of anaphylaxis. Our data also show that MC-deficient (KitW/KitW-v) mice did not suffer, unlike their littermate controls, anaphylactic reactions despite the fact that serum levels of peanut-specific Igs were similarly elevated. Finally, FcεRI-deficient mice experienced anaphylactic responses although to a significantly lesser degree than those observed in WT mice. Thus, these data demonstrate that the presence of peanut-specific Abs along with functional MCs comprise a necessary and sufficient condition for the elicitation of peanut-induced anaphylaxis. That the absence of FcεRI prevented the development of anaphylaxis only partially insinuates the contribution of an IgE-independent pathway, and suggests that strategies to impair MC degranulation may be necessary to improve the efficacy of anti-IgE therapy.

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Section: Discussionmentioning

confidence: 99%

Impact of CD40 Ligand, B Cells, and Mast Cells in Peanut-Induced Anaphylactic Responses

Sun

Arias

Álvarez

et al. 2007

The Journal of Immunology

106

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“…The oral mode of delivery has the potential to confer long-term mucosal immunity against pathogens such as HIV-1 if it can induce antigen specific cells to home to the gut as shown in previous studies [25][26][27][28], but efforts to stimulate immunity through this route may inadvertently induce oral tolerance instead [29]. Oral vaccine development using replication defective adenovirus, such as the vector we have tested, may be impeded by vector instability in the acidic environment of the stomach, through which it must pass to ensure antigen presentation and maximum exposure to and uptake by the antigen presenting cells of the intestine.…”

Section: Discussionmentioning

confidence: 99%

Intramuscular rather than oral administration of replication-defective adenoviral vaccine vector induces specific CD8+ T cell responses in the gut

Lin

Cun

Harris-McCoy

et al. 2007

Vaccine

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Gut-associated lymphoid tissue (GALT) is the primary replication site for HIV-1, resulting in a pronounced CD4 + T cell loss in this tissue during primary infection. A mucosal vaccine that generates HIV-specific CD8 + T cells in the gut could prevent the establishment of founder populations and broadcasting of virus. Here, we immunized mice orally and systemically with a chimpanzee derived adenoviral vector expressing HIV gag (AdC68gag) and measured frequencies of gag-specific interferon-gamma (IFN-γ) producing CD8 + T cells in the GALT. A single oral administration was inefficient at eliciting responses in the mesenteric lymph nodes and Peyer's Patches, while a single intramuscular administration elicited strong systemic and detectable mucosal responses. The gagspecific CD8 + T cell responses were present in both acute and memory phases following intramuscular administration.

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“…This is, in part, accomplished by the acquisition of differential homing instructions, including, but not limited to, unique adhesion molecules (30 -32) and chemoattractant receptors (25)(26)(27)(28)(29) that direct lymphocytes to tissues in which they are most likely to re-encounter their cognate Ag. Indeed, memory/effector T cells have been identified that selectively home to cutaneous (45)(46)(47) and various mucosal (30,31,33) tissues. Whether this tissue-selective paradigm is also evoked during tolerance induction is unknown.…”

Section: Discussionmentioning

confidence: 99%

Inhalation Tolerance Is Induced Selectively in Thoracic Lymph Nodes but Executed Pervasively at Distant Mucosal and Nonmucosal Tissues

Álvarez

Świrski

Yang

et al. 2006

The Journal of Immunology

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Under immunogenic conditions, both the site of initial Ag exposure and consequent T cell priming in specific draining lymph nodes (LNs) imprint the ensuing immune response with lasting tissue-selective tropism. With respect to immune tolerance, whether the site of tolerance induction leads to compartmentalized or, alternatively, pervasive tolerance has not been formally investigated. Using a murine model of inhalation tolerance, we investigated whether the induction of respiratory mucosal tolerance precludes the development of de novo Th2 sensitization upon subsequent exposure to the same Ag at distant mucosal (gut) and nonmucosal (cutaneous) sites. By tracking the proliferation of CFSE-labeled OVA-TCR transgenic CD4+ T cells upon OVA inhalation in vivo, we defined the site of tolerance induction to be restricted to the thoracic LNs. Expectedly, inhalation tolerance prevented de novo Th2 sensitization upon subsequent exposure to the same Ag at the same site. Importantly, although gut- and skin-draining LNs were not used during tolerance induction, de novo Ag-specific proliferation and Th2 differentiation in these LNs, as well as memory/effector Th2 responses in the gut (allergic diarrhea) and skin (late-phase cutaneous responses) were inhibited upon immunogenic challenge to the same Ag. Interestingly, this pervasive tolerogenic phenotype was not associated with the presence of suppressive activity throughout the lymphatics; indeed, potent suppressive activity was detected solely in the spleen. These data indicate that while inhalation tolerance is selectively induced in local thoracic LNs, its tolerogenic activity resides systemically and leads to pervasive immune tolerance in distant mucosal and nonmucosal sites.

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Expression of mucosal homing receptor alpha4beta7 by circulating CD4+ cells with memory for intestinal rotavirus.

Cited by 137 publications

References 21 publications

Impact of CD40 Ligand, B Cells, and Mast Cells in Peanut-Induced Anaphylactic Responses

Impact of CD40 Ligand, B Cells, and Mast Cells in Peanut-Induced Anaphylactic Responses

Intramuscular rather than oral administration of replication-defective adenoviral vaccine vector induces specific CD8+ T cell responses in the gut

Inhalation Tolerance Is Induced Selectively in Thoracic Lymph Nodes but Executed Pervasively at Distant Mucosal and Nonmucosal Tissues

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