Analysis of Monocyte Chemotactic Protein-1 Production in Different Major Histocompatability Complex-Restricted Antigen Presentation Systems

Tekstra, Janneke; Tjin, Esther P.M.; Tuk, Cornelis W.; Broekhuis-Fluitsma, Donna M.; Havenith, Carin E.G.; Beelen, Robert H.J.

doi:10.1006/clim.2001.5090

Cited by 2 publications

(2 citation statements)

References 20 publications

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“…Moreover, CCL16 induced macrophages to release downstream CCL2 and CCL5 chemokines and proinflammatory cytokines, such as IL-1␤, TNF-␣, and markedly, IL-12. The singularly high levels of CCL2 secreted are in agreement with data showing that the APCs, which most effectively induce a T cell response, are those that produce elevated amounts of CCL2 [32]. The enhanced release of chemokines and cytokines induced by CCL16 in macrophages may stimulate and protract the inflammatory response and thus enhance acquired and innate immunity.…”

Section: Discussionsupporting

confidence: 85%

CCL16/LEC powerfully triggers effector and antigen-presenting functions of macrophages and enhances T cell cytotoxicity

Cappello¹,

Caorsi²,

Bosticardo³

et al. 2003

Journal of Leukocyte Biology

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The human CC chemokine CCL16, a liver-expressed chemokine, enhances the killing activity of mouse peritoneal macrophages by triggering their expression of tumor necrosis factor alpha (TNF-alpha) and Fas ligand. Macrophages also respond to CCL16 by enhancing their production of monocyte chemoattractant protein-1, regulated on activation, normal T cells expressed and secreted chemokines, and interleukin (IL)-1 beta, TNF-alpha, and IL-12. The effect of CCL16 is almost as strong as that of lipopolysaccharide and interferon-gamma, two of the best macrophage activators. Moreover, CCL16-activated macrophages overexpress membrane CD80, CD86, and CD40 costimulatory molecules and extensively phagocytose tumor cell debris. On exposure to such debris, they activate a strong, tumor-specific, cytolytic response in virgin T cells. Furthermore, cytolytic T cells generated in the presence of CCL16 display a higher cytotoxicity and activate caspase-8 in tumor target cells. This ability to activate caspase-8 depends on their overexpression of TNF-alpha and Fas ligand induced by CCL16. These data reveal a new function for CCL16 in the immune-response scenario. CCL16 significantly enhances the effector and the antigen-presenting function of macrophages and augments T cell lytic activity.

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Section: Discussionsupporting

confidence: 85%

CCL16/LEC powerfully triggers effector and antigen-presenting functions of macrophages and enhances T cell cytotoxicity

Cappello¹,

Caorsi²,

Bosticardo³

et al. 2003

Journal of Leukocyte Biology

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“…In murine IPS, the highest levels of CCL2 are produced after allogeneic BMT in a T celldependent manner (29). In vitro studies have shown that high amounts of CCL2 are produced by antigen-presenting cells (APC) that are effective inducers of T cell responses (34). The major receptor for CCL2 is CC chemokine receptor 2 (CCR2), present on monocytes, and, in rodent systems, this interaction has been shown to play a crucial role in monocyte/macrophage recruitment in inflammation, autoimmunity, and resistance to infectious organisms (16,20,21,24,35,38,39).…”

mentioning

confidence: 99%

Post-BMT lung injury occurs independently of the expression of CCL2 or its receptor, CCR2, on host cells

Panoskaltsis‐Mortari¹,

Hermanson²,

Taras³

et al. 2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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Idiopathic pneumonia syndrome (IPS) is a significant cause of mortality post-bone marrow transplant (BMT) in humans. In our murine model, lethal pre-BMT conditioning and allogeneic T cells result in the recruitment of host antigen-presenting cells (APC) and donor T cells into the lung post-BMT concomitant with development of severe lung dysfunction. CCL2 induction is found in bronchoalveolar lavage fluid (BALF) before host monocyte influx. The major receptor for CCL2 is CCR2 present on monocytes; this interaction can play a crucial role in monocyte recruitment in inflammation. To determine whether blockade of the CCL2/CCR2 pathway could hinder host monocyte influx, lethally conditioned wild-type (WT), CCL2(-/-), or CCR2(-/-) mice were transplanted with allogeneic marrow and spleen cells. WT and (-/-) recipients exhibited equivalent lung dysfunction post-BMT. The frequencies of host macrophages as well as donor CD4(+) and CD8(+) T cells in lungs post-BMT did not differ between WT and (-/-) recipients. However, the T cell dependency of the host CD11b(+) major histocompatibility complex class II(+) cell influx was lost in CCR2(-/-) recipients. In CCR2(-/-) mice, this influx was accompanied by elevated levels of CCL20. Post-BMT BALF and sera of (-/-) mice did not reveal any decrease in cytokines or chemokines compared with WT mice. CCL2(-/-) mice had a deficiency of CCL2 in their BALF and sera post-BMT, confirming our hypothesis that CCL2 is predominantly host derived. Therefore, IPS can occur independently of host expression of CCL2 or CCR2, and compensatory mechanisms exist for regulating APC recruitment into the lung during the early post-BMT period.

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Analysis of Monocyte Chemotactic Protein-1 Production in Different Major Histocompatability Complex-Restricted Antigen Presentation Systems

Cited by 2 publications

References 20 publications

CCL16/LEC powerfully triggers effector and antigen-presenting functions of macrophages and enhances T cell cytotoxicity

CCL16/LEC powerfully triggers effector and antigen-presenting functions of macrophages and enhances T cell cytotoxicity

Post-BMT lung injury occurs independently of the expression of CCL2 or its receptor, CCR2, on host cells

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