Identification of IL-16 as the lymphocyte chemotactic activity in the bronchoalveolar lavage fluid of histamine-challenged asthmatic  patients

Mashikian, Margaret Vallen; Tarpy, Robert; Saukkonen, Jussi; Lim, Kaiser G.; Fine, Gregg; Cruikshank, William W.

doi:10.1016/s0091-6749(98)70403-8

Cited by 51 publications

(32 citation statements)

References 20 publications

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“…Its presence in high concentrations in alveolar lavages of asthmatic patients and its ability to induce the production of proinflammatory cytokines suggests a role in inflammation (8,9). IL-16 has also been shown to inhibit HIV replication and acts as a chemoattractant factor (4,6).…”

Section: Discussionmentioning

confidence: 99%

Cutting Edge: CD4 Is Not Required for the Functional Activity of IL-16

Mathy

Bannert

Norley

et al. 2000

The Journal of Immunology

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IL-16 functions as a chemoattractant factor, inhibitor of HIV replication, and inducer of proinflammatory cytokine production. Previous studies have suggested that CD4 is the receptor for IL-16, because only CD4+ cells respond to IL-16 and both the anti-CD4 Ab OKT4 and soluble CD4 can block IL-16 function. However, these are only indirect evidence of a requirement for CD4, and to date a direct interaction between IL-16 and CD4 has not been shown. In this paper, we report that cells from CD4 knockout mice are as responsive to IL-16 as their CD4 wild-type equivalents in both assays testing for IL-16 function (chemotaxis and production of proinflammatory cytokines). In addition, the inhibitory effect of soluble CD4 on IL-16 function observed using CD4 wild type murine cells was not observed using CD4 knockout cells. These data demonstrate that CD4 is not required for IL-16 function and suggest that another molecule acts as the major receptor.

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Section: Discussionmentioning

confidence: 99%

Cutting Edge: CD4 Is Not Required for the Functional Activity of IL-16

Mathy

Bannert

Norley

et al. 2000

The Journal of Immunology

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“…Fluorescein-conjugated anti-CXCR4 Ab was purchased from PharMingen (San Diego, CA). Unconjugated anti-IL-16 Ab (clone 14.1) was isolated from hybridoma supernatants, purified using protein A affinity chromatography, and used at a concentration of 5 g/ml, which is sufficient to neutralize 10 Ϫ10 M rIL-16-induced migration of human T cells (23). HIV-1 gp120 IIIB was purchased from Intracel (Issaquah, WA).…”

Section: Cytokines and Absmentioning

confidence: 99%

Desensitization of CXC Chemokine Receptor 4, Mediated by IL-16/CD4, Is Independent of p56lckEnzymatic Activity

Drenth

Jenkins

Ledwich

et al. 2000

The Journal of Immunology

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CCR5 and CXC chemokine receptor 4 (CXCR4) are coreceptors for CD4 as defined by HIV-1 glycoprotein (gp) 120 binding. Pretreatment of T cells with gp120 results in modulation of both CCR5 and CXCR4 responsiveness, which is dependent upon p56lck enzymatic activity. The recent findings that pretreatment of T cells with a natural CD4 ligand, IL-16, could alter cellular responsiveness to macrophage-inflammatory protein-1β (MIP-1β) stimulation, prompted us to investigate whether IL-16 could also alter CXCR4 signaling. These studies demonstrate that IL-16/CD4 signaling in T lymphocytes also results in loss of stromal derived factor-1α (SDF-1α)/CXCR4-induced chemotaxis; however, unlike MIP-1β/CCR5, the effects were not reciprocal. There was no effect on eotaxin/CCR3-induced chemotaxis. Desensitization of CXCR4 by IL-16 required at least 10–15 min pretreatment; no modulation of CXCR4 expression was observed, nor was SDF-1α binding altered. Using murine T cell hybridomas transfected to express native or mutated forms of CD4, it was determined that IL-16/CD4 induces a p56lck-dependent inhibitory signal for CXCR4, which is independent of its tyrosine catalytic activity. By contrast, IL-16/CD4 desensitization of MIP-1β/CCR5 responses requires p56lck enzymatic activity. IL-16/CD4 inhibition of SDF-1α/CXCR4 signals requires the presence of the Src homology 3 domain of p56lck and most likely involves activation of phosphatidylinositol-3 kinase. These studies indicate the mechanism of CXCR4 receptor desensitization induced by a natural ligand for CD4, IL-16, is distinct from the inhibitory effects induced by either gp120 or IL-16 on CCR5.

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“…However, eosinophils also comprise a potential cellular source of IL-16 [8]. This cytokine plays an important role in airway hyperresponsiveness and upregulation of IgE [9] and appears in the asthmatic airways, where it contributes to the early infiltration of Th cells and eosinophils [10]. Recently it could be demonstrated that IL-16 is also a potent chemoattractant for dendritic cells, which are the major antigen-presenting cells and initiators of an adaptive immune response [11].…”

Section: Introductionmentioning

confidence: 99%

Neuropeptide-Induced Inhibition of IL-16 Release from Eosinophils

Dunzendorfer

Feistritzer

Enrich

et al. 2002

Neuroimmunomodulation

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Objectives: Eosinophils are prominent inflammatory cells that respond to peripheral neuropeptides in vitro and in vivo. At inflammatory sites, cytokines activate distinct cellular and biochemical pathways that act in a coordinated fashion. We investigated whether peripheral neuropeptides can act as immunomodulators by influencing cytokine release from eosinophils. Methods: Human eosinophils were enriched using magnetic cell sorting, and IL-16 levels in supernatants from maintained eosinophils were measured by ELISA. Biological activity of IL-16 was confirmed in lymphocyte chemotaxis assays. Results: Substance P, vasoactive intestinal polypeptide, calcitonin gene-related peptide and secretoneurin reduced the IL-16 release from eosinophils; this effect was additive to that observed with GM-CSF or IL-5. Decreased IL-16 levels in supernatants resulted in reduced lymphocyte chemotaxis, whereas supernatants derived from SP-treated eosinophils stimulated lymphocyte chemotaxis, even though IL-16 was decreased. Conclusions: Results suggest that distinct neuropeptides are able to reduce the number of lymphocytes at inflammatory sites during existing eosinophilia by inhibiting eosinophil IL-16 release, thus attenuating the pro-inflammatory action of lymphocytes and monocytes.

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Identification of IL-16 as the lymphocyte chemotactic activity in the bronchoalveolar lavage fluid of histamine-challenged asthmatic patients

Cited by 51 publications

References 20 publications

Cutting Edge: CD4 Is Not Required for the Functional Activity of IL-16

Cutting Edge: CD4 Is Not Required for the Functional Activity of IL-16

Desensitization of CXC Chemokine Receptor 4, Mediated by IL-16/CD4, Is Independent of p56lckEnzymatic Activity

Neuropeptide-Induced Inhibition of IL-16 Release from Eosinophils

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