Localization of Th-cell subsets in inflammation: differential thresholds for extravasation of Th1 and Th2 cells

D’Ambrosio, Daniele; Iellem, Andrea; Colantonio, Lucia; Clissi, Barbara; Pardi, Ruggero; Sinigaglia, Francesco

doi:10.1016/s0167-5699(00)01590-5

Cited by 72 publications

(55 citation statements)

References 37 publications

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“…In addition to PSGL-1, certain integrins likely to be important for passage across the endothelium have also been reported to be differentially expressed on Th1 and Th2 cells (72,73). We have shown ␣ L ␤ 2 (LFA-1), a receptor for ICAM-1, at higher levels on IFN-␥-producing, Th1-like cells.…”

Section: Discussionmentioning

confidence: 67%

Recruitment of IFN-γ-Producing (Th1-Like) Cells into the Inflamed Retina In Vivo Is Preferentially Regulated by P-Selectin Glycoprotein Ligand 1:P/E-Selectin Interactions

Manivannan

Jiang

et al. 2004

The Journal of Immunology

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Although there is evidence that altering the Th1/Th2 balance toward Th2 cells may be important in the resolution of Th1-type autoimmune disease, adoptive transfer of Th2 cells is not effective in protecting against Th1-type disease and may cause disease. Therefore, we examined the recruitment of Th1- and Th2-like cells into the retina in the murine autoimmune disease experimental autoimmune uveoretinitis. CD4 T cells were polarized in vitro to IFN-γ-producing Th1-like cells and non-IFN-γ-producing Th2-like cells, labeled, and adoptively transferred. Trafficking to the retina in vivo was evaluated by scanning laser ophthalmoscopy and infiltration by confocal microscopy. There were more rolling and adherent Th1-like cells and they rolled more slowly than did Th2-like cells. Th1-like cells were preferentially recruited into the retinal parenchyma at both initiation and resolution. Surface P-selectin glycoprotein ligand 1 (PSGL-1) and LFA-1 were up-regulated on both populations but were expressed at higher levels on Th1-like cells. Up-regulation of CD44 expression was higher on Th2-like cells. P-selectin, E-selectin, and ICAM-1 are up-regulated on postcapillary venules in the retina. Pretreatment of Th1-like cells with anti-PSGL-1 inhibited rolling and infiltration of Th1-like cells but not Th2-like cells, providing direct in vivo evidence for the inability of Th2 to respond to P/E-selectin despite increased expression of PSGL-1. Anti-LFA-1 pretreatment inhibited infiltration of both Th1- and Th2-like cells, but more so Th-1. We suggest that random trafficking of activated T cells (both Th1 and Th2) across the blood-retina barrier is mediated by CD44:CD44R and LFA-1:ICAM-1, whereas preferential recruitment of Th1 cells is mediated by PSGL-1:P/E-selectin.

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Section: Discussionmentioning

confidence: 67%

Recruitment of IFN-γ-Producing (Th1-Like) Cells into the Inflamed Retina In Vivo Is Preferentially Regulated by P-Selectin Glycoprotein Ligand 1:P/E-Selectin Interactions

Manivannan

Jiang

et al. 2004

The Journal of Immunology

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“…Conversely, the CC chemokines macrophage-derived chemokine (MDC, CCL22) and thymus and activation-regulated chemokine (TARC, CCL17) are preferential attractants for polarized Th2 cells that express CCR4 (15). MDC production is induced by IL-4 and IL-13 and inhibited by IFNs and IL-12 (17)(18)(19)(20)(21). These studies have outlined the existence of chemokinebased circuits that induce and sustain polarized type I and type II responses (2,20).…”

mentioning

confidence: 99%

Fractalkine (CX3CL1) as an amplification circuit of polarized Th1 responses

Fraticelli¹,

Sironi²,

Bianchi³

et al. 2001

J. Clin. Invest.

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289

240

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Fractalkine (FKN, CX3CL1) is a membrane-bound CX3C chemokine induced by primary proinflammatory signals in vascular endothelial cells (ECs). Here we examined the role of FKN in polarized Th1 or Th2 responses. Proinflammatory signals, including LPS, IL-1, TNF, and CD40 ligand, induced FKN, as did IFN-γ, which had synergistic activity with TNF. IL-4 and IL-13 did not stimulate the expression of FKN and markedly reduced induction by TNF and IFN-γ. TNF alone or combined with IFN-γ also induced release of soluble FKN, which was inhibited by IL-4 and IL-13. In light of this differential regulation of FKN by the master cytokines that control polarized responses, we analyzed the interaction of FKN with natural killer (NK) cells and polarized T-cell populations. NK cells expressed high levels of the FKN receptor CX3CR1 and responded to FKN. CX3CR1 was preferentially expressed in Th1 compared with Th2 cells. Th1 but not Th2 cells responded to FKN. By immunohistochemistry, FKN was expressed on ECs in psoriasis, a Th1-dominated skin disorder, but not in Th2-driven atopic dermatitis. Similarly, ECs in Mycobacterium tuberculosis granulomatous lymphadenitis, but not those in reactive lymph node hyperplasia or in Castelman's disease, showed immunoreactive FKN. These results indicate that regulated expression of FKN in ECs participates in an amplification circuit of polarized type I responses

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“…In all of these tissues, Th1 cells are found in substantially higher numbers than Th2 cells. D'Ambrosio et al (13) have suggested that this means that Th2 cells have a higher threshold for entry into effector sites than do Th1 cells. Th1 cells and Th2 cells manifest differential expression of many adhesion receptors.…”

mentioning

confidence: 99%

Antigen-Nonspecific Recruitment of Th2 Cells to the Lung as a Mechanism for Viral Infection-Induced Allergic Asthma

Stephens

Randolph

Huang

et al. 2002

The Journal of Immunology

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Respiratory viral infections have been shown to trigger exacerbations of asthma; however, the mechanism by which viral Th1-type inflammation exacerbates an allergic Th2-type disease remains unclear. We have previously shown that although adoptively transferred Th2 cells are inefficiently recruited to the lung in response to Ag, cotransfer of Th1 cells can increase accumulation of Th2 cells. In this study, we show that respiratory viral infection increases recruitment of resting Th2 cells specific for OVA even in the absence of OVA challenge. These findings suggest that the mechanism by which Th1-type inflammation enhances allergy is via an effect on recruitment. To study the role of the antigenic specificity of Th1 cells in the enhancement of Th2 cell recruitment and to determine whether virus-induced recruitment of OVA-specific Th2 cells may involve Th1 cells specific to a different Ag, we tested whether hen egg lysozyme-specific Th1 cells could synergize with OVA-specific Th2 cells. Challenge of mice that had received adoptively transferred Th1 cells plus Th2 cells induced the expression of inflammatory chemokines in the lung and increased both recruitment and activation of Th2 cells, leading to eosinophil recruitment, even in the absence of challenge with the Th2 Ag. Interestingly, as IL-5 supports eosinophilia, culture of resting Th2 cells with fresh APC induced production of IL-5 in the absence of specific Ag. Thus, Ag-specific activation of Th1 cells enhances the recruitment potential of the lung leading to recruitment and activation of Th2 cells. This implies that circulating Th2 cells in allergic individuals could enter the lungs in response to infection or inflammation and become activated to trigger allergy.

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Localization of Th-cell subsets in inflammation: differential thresholds for extravasation of Th1 and Th2 cells

Cited by 72 publications

References 37 publications

Recruitment of IFN-γ-Producing (Th1-Like) Cells into the Inflamed Retina In Vivo Is Preferentially Regulated by P-Selectin Glycoprotein Ligand 1:P/E-Selectin Interactions

Recruitment of IFN-γ-Producing (Th1-Like) Cells into the Inflamed Retina In Vivo Is Preferentially Regulated by P-Selectin Glycoprotein Ligand 1:P/E-Selectin Interactions

Fractalkine (CX3CL1) as an amplification circuit of polarized Th1 responses

Antigen-Nonspecific Recruitment of Th2 Cells to the Lung as a Mechanism for Viral Infection-Induced Allergic Asthma

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