Splenic macrophage subsets and their function during blood-borne infections

被引:140
作者
da Silva, Henrique Borges [1 ]
Fonseca, Raissa [1 ]
Pereira, Rosana Moreira [1 ]
Cassado, Alexandra dos Anjos [1 ]
Alvarez, Jose Maria [1 ]
D'Imperio Lima, Maria Regina [1 ]
机构
[1] Univ Sao Paulo, Dept Immunol, Inst Ciencias Biomed, BR-05508000 Sao Paulo, Brazil
基金
巴西圣保罗研究基金会; 瑞典研究理事会;
关键词
spleen; macrophages; phagocytosis; pattern-recognition receptors; tissue remodeling; MARGINAL ZONE MACROPHAGES; RED PULP MACROPHAGES; PLASMODIUM-FALCIPARUM; SCAVENGER RECEPTORS; DC-SIGN; T-CELL; SPI-C; BINDING; ANTIGEN; SPLEEN;
D O I
10.3389/fimmu.2015.00480
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The spleen is one of the major immunological sites for maintaining blood homeostasis. Previous studies showed that heterogeneous splenic macrophage populations contribute in complimentary ways to control blood-borne infections and induce effective immune responses. Marginal metallophilic macrophages (MMM Phi s) and marginal zone macrophages (MZM Phi s) are cells with great ability to internalize blood-borne pathogens such as virus or bacteria. Their localization adjacent to T- and B-cell-rich splenic areas favors the rapid contact between these macrophages and cells from adaptive immunity. Indeed, MMM Phi s and MZM Phi s are considered important bridges between innate and adaptive immunity. Although red pulp macrophages (RpM Phi s) are mainly considered scavengers for senescent erythrocytes, several data indicate a role for RpM Phi s in control of infections such as blood-stage malaria as well as in the induction of innate and adaptive immunity. Here, we review current data on how different macrophage subsets recognize and help eliminate blood-borne pathogens, and, in turn, how the inflammatory microenvironment in different phases of infection (acute, chronic, and after pathogen clearance) influences macrophage function and survival.
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页数:9
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共 76 条
[51]  
MARODI L, 1991, J IMMUNOL, V146, P2783
[52]   Strain-specific spleen remodelling in Plasmodium yoelii infections in Balb/c mice facilitates adherence and spleen macrophage-clearance escape [J].
Martin-Jaular, Lorena ;
Ferrer, Mireia ;
Calvo, Maria ;
Rosanas-Urgell, Anna ;
Kalko, Susana ;
Graewe, Stefanie ;
Soria, Guadalupe ;
Cortadellas, Nuria ;
Ordi, Jaume ;
Planas, Anna ;
Burns, James ;
Heussler, Volker ;
del Portillo, Hernando A. .
CELLULAR MICROBIOLOGY, 2011, 13 (01) :109-122
[53]   Structure and function of the spleen [J].
Mebius, RE ;
Kraal, G .
NATURE REVIEWS IMMUNOLOGY, 2005, 5 (08) :606-616
[54]   Plasmodium chabaudi-infected erythrocytes adhere to CD36 and bind to microvascular endothelial cells in an organ-specific way [J].
Mota, MM ;
Jarra, W ;
Hirst, E ;
Patnaik, PK ;
Holder, AA .
INFECTION AND IMMUNITY, 2000, 68 (07) :4135-4144
[55]   Association of SIGNR1 with TLR4-MD-2 enhances signal transduction by recognition of LPS in gram-negative bacteria [J].
Nagaoka, K ;
Takahara, K ;
Yoshida, H ;
Steinman, RM ;
Saitoh, S ;
Akashi-Takamura, S ;
Miyake, K ;
Kang, YS ;
Park, CG ;
Inaba, K .
INTERNATIONAL IMMUNOLOGY, 2005, 17 (07) :827-836
[56]  
NAITO M, 1991, AM J PATHOL, V139, P657
[57]   Involvement of macrophage mannose receptor in the binding and transmission of HIV by macrophages [J].
Nguyen, DG ;
Hildreth, JEK .
EUROPEAN JOURNAL OF IMMUNOLOGY, 2003, 33 (02) :483-493
[58]   B cells are crucial for both development and maintenance of the splenic marginal zone [J].
Nolte, MA ;
Arens, R ;
Kraus, M ;
van Oers, MHJ ;
Kraal, G ;
van Lier, RAW ;
Mebius, RE .
JOURNAL OF IMMUNOLOGY, 2004, 172 (06) :3620-3627
[59]   Heat shock protein 60 is a putative endogenous ligand of the toll-like receptor-4 complex [J].
Ohashi, K ;
Burkart, V ;
Flohé, S ;
Kolb, H .
JOURNAL OF IMMUNOLOGY, 2000, 164 (02) :558-561
[60]   The extra domain A of fibronectin activates toll-like receptor 4 [J].
Okamura, Y ;
Watari, M ;
Jerud, ES ;
Young, DW ;
Ishizaka, ST ;
Rose, J ;
Chow, JC ;
Strauss, JF .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (13) :10229-10233