Mycobacteria-primed macrophages and dendritic cells induce an up-regulation of complement C5a anaphylatoxin receptor (CD88) in CD3+ murine T cells

Connelly, Mary Anne; Moulton, Rachel A.; Smith, Amanda K.; Lindsey, Devin R.; Sinha, Mala; Wetsel, Rick A.; Jagannath, Chinnaswamy

doi:10.1189/jlb.1005582

Cited by 19 publications

(16 citation statements)

References 34 publications

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“…BM DC, plasmacytoid DCs (pDCs)] [11,15,22], subsets of human DCs (i.e. monocyte-and skinderived DCs, pDCs) [23][24][25][26], T cells [14,15,[27][28][29] and stem cells [30,31]. Expression of C3aR on haematopoietic stem/progenitor cells has been shown to promote the trafficking/homing of these cells to the BM [30,31].…”

Section: C3ar and C5ar Expressionmentioning

confidence: 99%

The Role of Anaphylatoxins C3a and C5a in Regulating Innate and Adaptive Immune Responses

Peng

Li²,

Sacks³

et al. 2009

IADT

123

106

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C3a and C5a, the small (approximately 10KDa) cleavage fragments released by complement activation, are potent mediators of inflammation. They are anaphylatoxins and act as cell activators with nanomolar affinity, exerting their functions through binding to specific receptors (C3aR and C5aR or C5L2 respectively). Recent studies suggest that locally generated complement effector molecules including C3a and C5a contribute to pathological processes in inflammatory and immunological diseases as well as adaptive immune response besides its host defence mechanism. Targeting the receptors and/or their ligands can reduce undesired inflammatory responses and tissue damage in certain pathological conditions. In this article we describe the recent developments in this important area and focus on the role of C3a/C5a in inflammatory and autoimmune diseases and in adaptive immune responses.

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Section: C3ar and C5ar Expressionmentioning

confidence: 99%

The Role of Anaphylatoxins C3a and C5a in Regulating Innate and Adaptive Immune Responses

Peng

Li²,

Sacks³

et al. 2009

IADT

123

106

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“…Bone marrow derived macrophages (BMMs) were differentiated as previously described [39]. Briefly, cells were isolated from C57BL/6 mice (6 weeks, Jackson Laboratories, Bar Harbor, ME) by flushing the femur with McCoy's medium supplemented with 100 μg/mL penicillin G (Sigma) and 50 μg/mL gentamycin sulfate (Sigma).…”

Section: Derivation and Treatment Of Bone Marrow Derived Macrophagesmentioning

confidence: 99%

Influence of bovine lactoferrin on expression of presentation molecules on BCG-infected bone marrow derived macrophages

Hwang¹,

Kruzel

Actor³

2009

Biochimie

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The current vaccine for tuberculosis (TB), caused by Mycobacterium tuberculosis (MTB), is an attenuated strain of Mycobacterium bovis bacillus Calmette-Guerin (BCG). BCG has proven to be effective in children, however, efficacy wanes in adulthood. Lactoferrin, a natural protein with immunomodulatory properties, is a potential adjuvant candidate to enhance efficacy of BCG. These studies define bovine lactoferrin as an enhancer of the BCG vaccine, functioning in part by modulating macrophage ability to present antigen and stimulate T-cells. BCG-infected bone marrow derived macrophages (BMMs) cultured with bovine lactoferrin increased the number of MHC II + expressing cells. Addition of IFN-γ and lactoferrin to BCG-infected BMMs enhanced MHC II expressiona dna increased the ratio of CD86/CD80. Lactoferrin treated BCG-infected BMMs were able to stimulate an increase in IFN-γ production from presensitized CD3 + splenocytes. Together, these results demonstrate that bovine lactoferrin is capable of modulating BCG-infected macrophages to enhance T-cell stimulation through increased surface expression of antigen presentation and costimulatory molecules, which potentially explains the observed in vivo bovine lactoferrin enhancement of BCG vaccine efficacy to protect against virulent MTB infection.

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“…However, with constitutive expression of adhesion molecules such as E-and P-selectin in the skin, this mechanism may have less importance in this vascular bed (16 -18). In addition, C5a might act directly as a lymphocyte chemoattractant during the contact sensitivity response, because C5a receptor expression has been shown on T lymphocytes (19,20). A limiting factor to test these possibilities is that most techniques, including histology or standard intravital microscopy, are not sufficiently sensitive to detect and/or track the very few endogenous effector CD4 T cells that might infiltrate the tissue at early time points.…”

Section: Ontact Sensitivity (Cs)mentioning

confidence: 99%

Multichannel Fluorescence Spinning Disk Microscopy Reveals Early Endogenous CD4 T Cell Recruitment in Contact Sensitivity via Complement

Norman

Hulliger

Colarusso

et al. 2008

The Journal of Immunology

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Contact sensitivity (CS) is one of the primary in vivo models of T cell-mediated inflammation. The presence of CS-initiating CD4 T lymphocytes at the time of challenge is essential for transfer and full development of the late phase CS inflammatory response. From this observation investigators have speculated that early recruitment of CD4 T cells to the site of challenge must occur. Moreover, there must be rapid synthesis/release and disappearance of an important mediator during the first hours after hapten challenge. Using spinning disk confocal microscopy, we observed the very early effector events of the immune response. Simultaneous, real-time visualization of predominant neutrophil and extremely rare CD4 T cell trafficking in the challenged skin vasculature was noted (one rolling CD4 T cell for every 10–18 rolling and adherent neutrophils). We demonstrate that neutrophil adhesion during the early CS response was reduced in C5a receptor-deficient (C5aR−/−) mice or leukotriene B4 receptor antagonist-treated mice, whereas CD4 T cell recruitment was only inhibited in C5aR−/− mice. In line with these observations, leukocyte infiltration and the associated tissue damage were significantly reduced in C5aR−/− mice but not in leukotriene B4 receptor antagonist-treated wild-type mice 24 h after challenge. C5a receptor expression on T cells and not on tissue resident cells was important for the development of a CS response. Thus, by using spinning disk confocal microscopy we visualized the early events of an adaptive immune response and identified the rare but essential recruitment of CD4 T cells via the complement pathway.

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Mycobacteria-primed macrophages and dendritic cells induce an up-regulation of complement C5a anaphylatoxin receptor (CD88) in CD3+ murine T cells

Cited by 19 publications

References 34 publications

The Role of Anaphylatoxins C3a and C5a in Regulating Innate and Adaptive Immune Responses

The Role of Anaphylatoxins C3a and C5a in Regulating Innate and Adaptive Immune Responses

Influence of bovine lactoferrin on expression of presentation molecules on BCG-infected bone marrow derived macrophages

Multichannel Fluorescence Spinning Disk Microscopy Reveals Early Endogenous CD4 T Cell Recruitment in Contact Sensitivity via Complement

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