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Science, ISSN 0036-8075, 05/2016, Volume 352, Issue 6286, pp. 712 - 716
Journal Article
Journal of Immunology, ISSN 0022-1767, 09/2014, Volume 193, Issue 5, pp. 2519 - 2530
Journal Article
PLoS ONE, ISSN 1932-6203, 02/2013, Volume 8, Issue 2, pp. e57082 - e57082
Journal Article
Immunology Letters, ISSN 0165-2478, 2015, Volume 168, Issue 1, pp. 13 - 21
Highlights • Complement factor H binds to human macrophages via CD11b/CD18 and CD11c/CD18. • Factor H enhances Candida albicans and zymosan induced release of... 
Allergy and Immunology | Candida albicans | Fungal pathogen | Factor H | CR3 | Protease | Sap2 | Complement | Immune evasion | ACTIVATION | HUMAN NEUTROPHILS | DENDRITIC CELLS | BINDING-PROTEIN | IMMUNOLOGY | IDENTIFICATION | HUMAN POLYMORPHONUCLEAR LEUKOCYTES | COMPLEMENT FACTOR-H | GENE FAMILY | EXPRESSION | HUMAN-MONOCYTES | CD18 Antigens - immunology | Humans | Macrophage-1 Antigen - immunology | CD11c Antigen - immunology | Host-Pathogen Interactions - immunology | Integrin alphaXbeta2 - immunology | CD11c Antigen - metabolism | CD11b Antigen - genetics | Integrin alphaXbeta2 - metabolism | CD11c Antigen - genetics | Fungal Proteins - immunology | RNA Interference | Integrin alphaXbeta2 - genetics | Candida albicans - physiology | Macrophage-1 Antigen - metabolism | Aspartic Acid Endopeptidases - immunology | Cytokines - immunology | Complement Factor H - immunology | CD11b Antigen - immunology | Cytokines - metabolism | Enzyme-Linked Immunosorbent Assay | CD18 Antigens - genetics | Cells, Cultured | Candida albicans - immunology | Blotting, Western | CD18 Antigens - metabolism | Complement Factor H - metabolism | Macrophage-1 Antigen - genetics | Aspartic Acid Endopeptidases - metabolism | Cell Line, Tumor | CD11b Antigen - metabolism | Candida albicans - enzymology | Fungal Proteins - metabolism | Index Medicus
Journal Article
Journal Article
European Journal of Immunology, ISSN 0014-2980, 2013, Volume 43, Issue 2, pp. 416 - 426
IL-1 drives Th responses, particularly Th17, in host defense. Sharing the same co-receptor, the IL-1 family member IL-36 exhibits properties similar to those... 
h responses | 36 | Pattern recognition | 36 receptor antagonist | IL-36 | IL-36 receptor antagonist | Th responses | GENERALIZED PUSTULAR PSORIASIS | IMMUNOLOGY | IMMUNE RECOGNITION | FUNGAL-INFECTIONS | BETA-GLUCAN RECEPTOR | INVASIVE ASPERGILLOSIS | CANDIDA-ALBICANS | IL-18 | IN-VIVO | CRITICALLY-ILL PATIENTS | T-CELLS | Forkhead Transcription Factors - immunology | Toll-Like Receptor 2 - genetics | Humans | Interleukin-17 - immunology | Lectins, C-Type - immunology | Macrophage-1 Antigen - immunology | Interferon-gamma - metabolism | Lectins, C-Type - genetics | Th1 Cells - immunology | Receptors, Interleukin - metabolism | Th1 Cells - metabolism | Lectins, C-Type - metabolism | Signal Transduction - immunology | Th17 Cells - metabolism | Forkhead Transcription Factors - metabolism | Aspergillosis - metabolism | Macrophage-1 Antigen - metabolism | Interferon-gamma - genetics | Spores, Fungal - immunology | Receptors, Interleukin - immunology | RNA, Messenger - genetics | Aspergillosis - genetics | Interleukin-17 - genetics | Toll-Like Receptor 4 - genetics | Signal Transduction - genetics | Toll-Like Receptor 4 - immunology | Toll-Like Receptor 2 - metabolism | Forkhead Transcription Factors - genetics | Receptors, Interleukin - genetics | Toll-Like Receptor 4 - metabolism | Hyphae - immunology | Interleukin-17 - metabolism | Macrophage-1 Antigen - genetics | Aspergillus fumigatus - immunology | Interferon-gamma - immunology | Aspergillosis - microbiology | Th17 Cells - immunology | Toll-Like Receptor 2 - immunology | Aspergillosis - immunology | RNA | Fungi | Composting | Index Medicus
Journal Article
Annals of the Rheumatic Diseases, ISSN 0003-4967, 12/2012, Volume 71, Issue 12, pp. 2028 - 2034
Journal Article
American Journal of Physiology - Regulatory, Integrative and Comparative Physiology, ISSN 0363-6119, 06/2006, Volume 290, Issue 6, pp. 1488 - 1495
The study evaluates the influence of monocytes/macrophages in the mechanisms of skeletal muscle injury using a mouse model and selective depletion of... 
Inflammation | Gene expression | Skeletal muscle injury | Myogenesis | CELLS | ACTIVATION | PHYSIOLOGY | MECHANISM | skeletal muscle injury | INJURY | ELIMINATION | PROLIFERATION | REPAIR | inflammation | DIFFERENTIATION | myogenesis | EXPRESSION | gene expression | Immunohistochemistry | Tumor Necrosis Factor-alpha - metabolism | Clodronic Acid - pharmacology | Gene Expression - drug effects | Gene Expression - genetics | MyoD Protein - genetics | Tumor Necrosis Factor-alpha - genetics | Muscle, Skeletal - metabolism | Insulin-Like Growth Factor I - genetics | Muscle, Skeletal - injuries | Myogenin - genetics | Cell Nucleus - metabolism | Monocytes - pathology | Antigens, Differentiation - metabolism | Female | Macrophage-1 Antigen - metabolism | Chemokine CCL2 - metabolism | Receptors, Chemokine - genetics | Insulin-Like Growth Factor Binding Proteins - genetics | Macrophages - pathology | Mice, Inbred C57BL | Receptors, Chemokine - metabolism | Chemokine CCL2 - genetics | MyoD Protein - metabolism | Regeneration - physiology | Reverse Transcriptase Polymerase Chain Reaction | Monocytes - drug effects | Regeneration - drug effects | Animals | Macrophage-1 Antigen - genetics | Muscle, Skeletal - physiopathology | Macrophages - drug effects | Antigens, Differentiation - genetics | Cell Nucleus - chemistry | Mice | Liposomes | Cell Nucleus - drug effects | Myogenin - metabolism | Index Medicus
Journal Article
Journal Article