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["Source Node","Target Node","Edge","Regulation","Explanation","References"]
["Mtb","Neutrophils","Mtb attracts neutrophils to the site of entry","activation","At the site of multiplication of bacilli, neutrophils are the first cells to arrive ","(Raja, 2004)"]
["Mtb","Macrophages","TLR, CR, MR and other receptors","activation","Bacilli take up residence in lung parenchyma, replicate in tissue macrophages and MDMs; (Mtb uses macrophage as its preferred habitat; Macrophages are endowed with several surface receptors ; The initial interaction with surface receptors influences the subsequent fate of Mtb within the macrophage); binding of the organism to the phagocyte through CR1, CR3, CR4, as well as MR and other cell surface receptor molecules","(Algood et al, 2003; Kaufmann, 2001; Schluger and Rom, 1998)"]
["Mtb","Dendritic Cells","TLR, CR, MR and other receptors","activation","Mtb enters human monocyte-derived dendritic cells after binding to the lectin DC-specific intracellular adhesion molecule-3 grabbing non-integrin (DC-SIGN); The multiplicity of existing phagocytic receptors, their ability to cross-talk, the presence of more than one receptor available for the internalization of the pathogen and their uneven distribution among cells and cell-type introduce a high level of complexity; Immature DC – Mtb phagocytosis, enhanced microbicidal property; Early interactions between lung dendritic cells (LDC) and Mtb are thought to be critical for mounting a protective, anti-mycobacterial immune response and for determining the outcome of the infection; ","(Basu, 2004; Bhatt and Salgame, 2007; Herrmann and Lagrange, 2005)"]
["Neutrophils","Activated Neutrophils","signaling molecules","activation","Neutrophils become activated upon stimulation","(Goldsby RA, 2004)"]
["Activated Neutrophils","Macrophages","TNF-α","activation","Neutrophils are thought to contribute to the control of infection through the production of chemokines, the induction of granuloma formation and the transferance of their own microbial molecules to infected macrophages;  Non-opsonic entrance of mycobacteria (pathogenic or non-pathogenic) in neutrophils elicits an oxidative burst and the release of specific granule proteins; Early after infection, there is also an influx of neutrophils in the lung","(Algood et al, 2003; Hernandez-Pando R, 2007; Velasco-Velázquez et al, 2003)"]
["Macrophages","Phagocytosis","entry via sinking (CR) or formation of pseudopodia (other receptors)","activation","Polysaccharide-mediated binding to CR3 provides a mode of binding that promotes CR3-directed phagocytosis;  (MBL induces phagocytosis directly through a yet undefined receptor or indirectly by activation of the complement system; When uptake by CRs and MR is blocked, bacilli are internalized through type A scavenger receptor); ","(Ehlers and Daffé, 1998; van Crevel et al, 2002)"]
["Phagocytosis","Pro-inflammatory cytokines","TLR1/TLR2, TLR2/TLR6, TLR4, TLR9","activation","Phagocytosis of the pathogen is the major stimulus to upregulation of cytokine gene regulation","(Goldsby RA, 2004)"]
["Phagocytosis","Activated phagocytic cells","CR, MR and other receptor signaling","activation","The macrophage mannose receptor appears to play an important role in the binding and phagocytosis of several human pathogens, but its phagocytic property and signaling pathways have been poorly defined; CR3-receptor activation leads rapidly to the association of the cytoplasmic domain o the receptor with cytoskeletal proteins; such as actinin, but as yet there is no evidence for a direct interaction between CR3 and downstream signaling proteins","(Goldsby RA, 2004; Le Cabec et al, 2005; May and Machesky, 2001)"]
["Phagocytosis","Cathelicidin","TLR1/TLR2","activation","TLR1/2 activation results in two differentially expressed candidate genes with known antimicrobial function, one of which was the Vitamin D receptor; ","(Liu et al, 2007)"]
["Cathelicidin","Mtb","inhibit growth","inhibition (of growth and survival of Mtb)","Antimicrobial peptide, Cathelicidin, significantly inhibits growth of Mtb","(Liu et al, 2007)"]
["Activated phagocytic cells","Pro-inflammatory cytokines","TNF, IL-1α, IL-1β, IL-6, GM-CSF ","activation","Macrophages are the first line of defence against mycobacteria, and when infected rapidly become activated and synthesize proinflammatory cytokines","(Moreno and Rees, 1993; Thakar et al, 2007)"]
["Pro-inflammatory cytokines","Activated phagocytic cells","TNF-α","activation","Cytokines and chemokines attract other inflammatory effector cells and activate them","(Raja, 2004; Schluger et al, 1998)"]
["Activated phagocytic cells","ROI and RNI","IFN-γ, TNF-α","activation","Phagocytes, upon activation by IFN- γ and TNF- α, generate NO and related RNI via iNOS2 using L-arginine as substrate; Activation of macrophage to exert its bactericidal or bacteriostatic effect is mediated by cytokines which trigger the production of ROI such as H2O2 and nitric oxide","(Andersen, 1997; Raja, 2004)"]
["ROI and RNI","Mtb","H2O2, nitric oxide","inhibition (of growth and survival of Mtb)","Phagosome acidification, lysosomal enzymes, ROI are the effector mechanisms by which macrophages combat resistant intracellular bacteria like Mtb; Phagosomal maturation is promoted by activation with IFN- γ, which stimulate anti-mycobacterial mechanisms in macrophages, notably ROI and RNI; H2O2 (ROI) – generated by macrophages via oxidative burst; Cell responses ( gene transcription and release of ROI and RNI) in turn promote phagocytosis and effective killing of bacteria","(Andersen, 1997; Ehlers et al, 1998; Kaufmann, 2001; Raja, 2004; Schluger et al, 1998)"]
["Phagocytosis","Mtb",null,"inhibition (of growth and survival of Mtb)"]
["Phagocytosis","T cells","TCRs, MHCs, adhesion molecules","activation (T cell stimulation in the presence of co-stimulatory molecules)","MHC-II molecules present mycobacterial proteins to Ag-specific CD4+ T cells","(Kaufmann, 2001; van Crevel et al, 2002)"]
["T cells","T cells","IL-2, IL-4, IL-6, IFN-γ, IFN-α","activation","The cytokines released by T cells can activate the T cells, forming an autocrine loop","Textbook"]
["Activated phagocytic cells","Activated Dendritic Cells","IL-1, TNF","activation","The cytokines released by activated phagocytic cells activate dendritic cells","(DeFranco et al, 2007)"]
["Activated phagocytic cells","NK cells","TNF-α, IL-15, IL-18","activation","IL-15 stimulates NK cell proliferation; IL-18 stimulates production of IFN-γ by NK cells","Textbook"]
["Dendritic Cells","Activated Dendritic Cells","signaling","activation","Dendritic cells are activated upon stimulation","(Goldsby RA, 2004)"]
["Activated Dendritic Cells","T cells","IL-12, IL-6, IL-18, IFN-α","activation","Dendritic cells, by assimilating signals from cytokines and from MO recognized by TLRs and C-type lectin receptors, can impart to differentiating T cells an imprint of the type of pathogen encountered in the periphery and are thus critical in linking the differentiation of specific T cell subsets with the distinct types of effector functions required for control of specific kinds of pathogens; Dendritic cells release Th1-inducing cytokines (IL-12, IFN-α)","(DeFranco et al, 2007; Marino and Kirschner, 2004)"]
["T cells","Th1 cells","IL-12, IL-18 (IFN-γ, IL-23, IL-27, GM-CSF)","activation","Currently, there are three well-defined cytokines that steer naïve T cells toward Th1 commitment - IL-12, IL-23, IL-27; Th1 cells express CCR5 and not CCR3; The differentiation of CD4+ T cells into Th1 cells is promoted by the early cytokine milieu, which includes IL-12, IL-18 and co-stimulatory molecules.","(Bhatt et al, 2007; DeFranco et al, 2007; Goldsby RA, 2004; Kaufmann, 2001)"]
["T cells","Th2 cells","IL-4 (IL-5, IL-10, TGF-β)","activation","The most potent determinant of polarized differentiation is the influence of IL-12 and IL-4 signaling, acting via Stat-4 and Stat-6, respectively for Th1 and Th2 cells; Th2 cells express CCR3 and not CCR5","(Bhatt et al, 2007; DeFranco et al, 2007; Reiner, 2001)"]
["T cells","γ/δ T cells ","cytokines","activation","T cells are differentiated into γ/δ T cells in the presence of stimulus like cytokines","(Goldsby RA, 2004)"]
["T cells","Tc cells","IL-4","activation","T cells in the presence of IL-4 can differentiate into Tc cells","(DeFranco et al, 2007)"]
["Activated Dendritic Cells","Tc cells","TCRs, MHCs, adhesion molecules","activation","Dendritic cells – take up pathogens and migrate to secondary lymphoid organs, where they present pathogen derived Ag to T lymphocytes; DCs but not macrophages can present exogenous Ags to CD8+ T lymphocytes via a cytosol-dependent pathway involving an unidentified phagosome-to-cytosol transporter","(Fortsch et al, 2000; Herrmann et al, 2005)"]
["Th1 cells","Th1 related cytokines","IFN-γ, TNF- α, IL-2, TNF-β, GM-CSF, IL-3","activation","Th1 cells are important in the control of TB infection due to their production of IFN- γ and TNF- α; Th1 cells produce IL-2, IFN- γ which are important in protective immunity","(Andersen, 1997; Goldsby RA, 2004; Raja, 2004)"]
["Th2 cells","Th2 related cytokines","IL-4, IL-5, IL-10, IL-13, IL-3, GM-CSF","activation","Th2 cells produce IL-4, IL-5, IL-10 which are involved in negative immune response; IL-4, IL-5, IL-13 are the signature cytokines of Th2 cells","(Goldsby RA, 2004; Raja, 2004; Reiner, 2001)"]
["Th1 related cytokines","Th2 related cytokines","IFN-γ (IL-2)","inhibition","Key cytokines produced by each subset negatively regulate the other subset","(Goldsby RA, 2004; Thakar et al, 2007)"]
["Th2 related cytokines","Th1 related cytokines","IL-10, IL-4 (IL-5)","inhibition","Key cytokines produced by each subset negatively regulate the other subset","(Goldsby RA, 2004; Thakar et al, 2007)"]
["Th2 related cytokines","Pro-inflammatory cytokines","IL-10, IL-4","inhibition","Some Th2 related cytokines can inhibit the production of pro-inflammatory cytokines","(Thakar et al, 2007)"]
["Tc cells","Tc related cytokines","IFN-γ, TNF- α, TNF-β","activation","Cytokines (Th1 like) are synthesized quickly upon recognition of antigen by the TCR; they act locally in most times and their action is specific, since they act on only those cells that express their receptor","Textbook"]
["Tc cells","Tc related cytotoxins","perforin, granulysin","activation","Tc cells have preformed cytotoxic effector molecules stored in cytoplasmic vesicles.  This is the most effective effector function of Tc cells.  Once their TCR recognised an infected cell, Tc cells release these vesicles in the narrow cleft in-between these two cells","Textbook"]
["Th1 related cytokines","Dendritic Cells","TNF-α, GM-CSF","activation","TNF-α acts as an important mediator of DC influx; Delivery of GM-CSF to the airways induces dramatic changes in the number and immunostimulatory capacity of airway and interstitial DCs","(Lambrecht et al, 2001; Thakar et al, 2007)"]
["Th2 related cytokines","Dendritic Cells","IL-4, IL-5, IL-13","activation","The Th2 related cytokines attract the dendritic cells to the site of infection","(Thakar et al, 2007)"]
["Th1 related cytokines","Macrophages","IFN-γ","activation","Macrophage activation is an important function of Th1 cells.  When Th1 cells get activated by an APC such as macrophage, they release IFN-γ, which is one of the signals to activate a macrophage","Textbook"]
["Th1 related cytokines","Tc cells","IFN-γ, IL-2","activation","Cytokines produced by Th1 cells activate macrophages and participate in the generation of Tc cells, resulting in a cell-mediated immune response","Textbook"]
["γ/δ T cells ","Apoptosis","IFN-γ","activation","Human γ/δ T cells are stimulated by a unique group of non-proteinaceous antigens that contain phosphate (phospholigands like prenyl phosphages and nucleotide conjugates).  Stimulated cells produce IFN-γ and express granule-dependent mycobactericidal activity; Other cells such as NK cells and γ/δ T cells may also contribute to control of TB, although this has not been definitively demonstrated in-vivo","(Algood et al, 2003; Kaufmann, 2001)"]
["Tc related cytokines","Activated phagocytic cells","IFN-γ, TNF- α","activation","IFN-γ and TNF- α are very important in the activation of macrophages and IFN-γ also induces the expression of MHC I on host cells, which will increase Ag presentation to CD8 T cells and thus infected cells are more readily destroyed","Textbook"]
["Tc cells","Apoptosis","Fas-FasL interactions","activation","Human T cells can induce target cell apoptosis throught two disntict pathways - secretion of cytolytic granules and Fas/FasL interactions","(Vergne et al, 2004)"]
["Tc related cytotoxins","Apoptosis","Perforin, Granulysin","activation","Upon release from Tc cell vesicles, perforins self assemble within the plasma membrane of the target cell, and from a pore, which can allow the passage of water, salt molecules (damage the target molecule to a limited extent) and other class of cytoxins, granulysin, into the target cell; Granulysin activates an intracellular protease pathway that eventually leads to apoptosis","(Goldsby RA, 2004)"]
["Apoptosis","Mtb","TNF- α","inhibition (of growth and survival of Mtb)","Macrophage apoptosis represents an innate defense mechanism linked to killing of intracellular mycobacteria; TNF- α is required for the induction of apoptosis in response to infection with Mtb; Apoptosis can be independent of Fas-FasL pathway; NuoG of Mycobacterium tuberculosis inhibits apoptosis.","(Basu, 2004; Canaday et al, 2001; van Crevel et al, 2002; Velmurugan et al, 2007)"]
["Th2 related cytokines","Eosinophils","IL-5, GM-CSF, IL-3, IL-4, IL-13","activation","At the site of infection, eosinophils are activated by Th2 related cytokines; ","(DeFranco et al, 2007; Lambrecht et al, 2001)"]
["Th2 related cytokines","Basophils","IL-4, IL-13, IL-5","activation","Th2 cells, identified by the release of IL-4, coordinate the immune responses by eosinophils, basophils and mast cells","(DeFranco et al, 2007; Medzhitov, 2007)"]
["Th2 related cytokines","Mast Cells","IL-3, IL-4, IL-10, IL-5, IL-13","activation","Th2 related cytokines act on mast cells and in turn activate them","(DeFranco et al, 2007; Medzhitov, 2007)"]
["Activated Mast Cells","Th2 related cytokines","IL-10","activation","Mast cells are critical for the development of Th2 response","(Hernandez-Pando R, 2007)"]
["Mast Cells","Activated mast cells","TLR signalling, IL-4, IL-5, IL-13","activation","Mast cells upon stimulation become activated mast cells","Textbook"]
["Eosinophils","Inflammatory molecules","ROI, IL-1, IL-2, IL-4, IL-5, IL-6, IL-8, IL-13, TNF-α, granules","activation","Following activation, eosinophil effector functions include production of ROI and cytokines","(DeFranco et al, 2007)"]
["Basophils","Inflammatory molecules","TNF-α, IL-4, ROI, granules","activation","Release potent inflammatory mediators like chemotactic factors, cytokines; Basophils express integrins as receptors for adhesion molecules","(DeFranco et al, 2007)"]
["Activated Mast Cells","Inflammatory molecules","TNF-α, IL-4, IL-5, IL-6, ROI, granules","activation","Release potent inflammatory mediators like chemotactic factors, cytokines","(DeFranco et al, 2007)"]
["Inflammatory molecules","Mtb","ROI, IL-1, IL-2, IL-4, IL-5, IL-6, IL-8, IL-13, TNF-α, granules","inhibition (of growth and survival of Mtb)","Inflammatory molecules released by cells such as Mast cells, eosinophils and basophils have the ability to kill the pathogen","(DeFranco et al, 2007)"]
["Th1 related cytokines","NK cells","IFN-γ, IL-2","activation","Cytokines produced by activated Th1 cells, particularly IL-2 and IFN-γ, also activate NK cells","(DeFranco et al, 2007)"]
["NK cells","T cells","IFN-γ, IL-32","activation","Before adaptive T cell immunity has fully developed, NK cells may be the main producers of IFN-γ, either in response to IL-12 and IL-18 or directly by exposure of mycobacterial oligodeoxynucleotides; Cells such as NK cells and γ/δ T cells may also contribute to control of TB, although this has not been definitively demonstrated in-vivo","(van Crevel et al, 2002)"]
["Dendritic Cells","NK cells","IL-12, IL-2, IL-15, IL-4, IFN-γ","activation","Microbially activated myeloid DCs produce chemokines and inflammatory cytokines, such as type I interferons, which in addition to IL-2, are involved in NK cell activation (in mice)","(Marino et al, 2004; Moretta, 2005)"]
["Activated Neutrophils","T cells","TNF-α","activation","The cytokines released by activated neutrophils can activate the naïve T cells","Textbook"]
["T cells","Neutrophils","IL-1, IL-4, IFN-γ, TNF-α, IL-8 (chemokine), TNF-β","activation","Recruits neutrophils; IL-8 activates neutrophils to degranulate and cause tissue damage","(Dinarello, 2000; Raja, 2004)"]
["Activated phagocytic cells","Fibroblasts","TNF, IL-1, TGF-β","activation","The tuberculous granuloma is made up of central caseous necrosis bordered by giant multinucleated cells, and surrounded by epitheloid cells aggregates, lymphocytes and fibroblasts","Textbook"]
["Activated phagocytic cells","Endothelial Cells","TNF, IL-1","activation","(IL-1 and TNF are inducers of endothelial adhesion molecules, which are essential for the adhesion of leuckocytes to the endothelial surface prior to emigration into the tissues; IL-1 and TNF initiate the cascade of inflammatory mediators by targeting the endothelium); The tuberculous granuloma is made up of central caseous necrosis bordered by giant multinucleated cells, and surrounded by epitheloid cells aggregates, lymphocytes and fibroblasts; activated endothelial cells express adhesion molecules like ICAM-1, ELAM-1, VCAM-1 on their cell surface; (within the granuloma, apoptosis is prominent in epitheloid cells)","(Dinarello, 2000; Raja, 2004)"]
["Macrophages","Th1 cells","CCL2, CCL5, CCL3, CCL4, IL-8","activation","Macrophages, when infected with M.tuberculosis, produce cytokines and chemokines; The chemokine gradient causes migration of cells to the infected macrophages, and a granuloma forms","(Algood et al, 2003; Basu, 2004; van Crevel et al, 2002)"]
["Macrophages","Th2 cells","CCL2, CCL5, CCL3, CCL4, IL-8","activation","Macrophages, when infected with M.tuberculosis, produce cytokines and chemokines; The chemokine gradient causes migration of cells to the infected macrophages, and a granuloma forms","(Algood et al, 2003; Basu, 2004; van Crevel et al, 2002)"]
["Macrophages","Activated phagocytic cells","CCL2, CCL5, CCL3, CCL4, IL-8","activation","Macrophages, when infected with M.tuberculosis, produce cytokines and chemokines; The chemokine gradient causes migration of cells to the infected macrophages, and a granuloma forms","(Algood et al, 2003; Basu, 2004; van Crevel et al, 2002)"]
["B cells","T cells","cytokines and chemokines","activation","B lymphocytes and Ab are not generally considered to be important in defense against tuberculosis.  However, B cells are present in large numbers in human and murine tuberculous granuloma.  These cells may contribute to pathology or granuloma formation by releasing cytokines or chemokines.  Absence of B cells resulted in fewer T cells trafficking to the lungs","(Algood et al, 2003)"]
["Activated phagocytic cells","T cells","IL-1, IL-6, IL-10, IL-12, IL-15, IL-18, IFN-γ, TNF-α, TNF-β, CXCL10, CCL3, CCL4, CCL5","activation","The cytokines released by activated phagocytic cells activate T cells","(Goldsby RA, 2004)"]
["T cells","Activated phagocytic cells","IL-1, IL-4, IFN-γ, TNF-α, IL-10, IFN-α, TNF-β","activation","Activated macrophages are the effector cells of cell mediated immunity; T cell stimuli for macrophage activation include CD40 ligand and cytokines, like IFN-γ","Textbook"]
["Activated phagocytic cells","Phagocytosis","increased phagocytic activity","activation","Increased phagocytic activity, increased expression of MHC-II","(Goldsby RA, 2004)"]
["T cells","Th17 cells","IL-1, IL-6, IL-23, TGF-β (?)","activation","IL-6 and TGF-β (for mice and not human) are required for the differentiation","(DeFranco et al, 2007; Korn et al, 2007; Laurence and O'Shea)"]
["Th17 cells","Th1 cells","CXCL9, CXCL10, CXCL11","activation","In mycobacterial infection, an early pathogen-specific Th17 response triggers the induction of chemokines like CXCL9, CXCL10, and CXCL11 that attract IFN-γ producing CD4+ Th1 cells into the lung parenchyma which eventually control the infection","(Korn et al, 2007)"]
["Th17 cells","Endothelial Cells","IL-17","activation","Th17 cells produce IL-17, which induces non-haematopoietic cell types, including epithelial cells, which produce chemokines to recruit neutrophils to the site of infection.","(Medzhitov, 2007)"]
["Phagocytosis","Anti-inflammatory cytokines","production of cytokines","activation","Macrophages release downregulating cytokines","(Goldsby RA, 2004)"]
["Anti-inflammatory cytokines","Pro-inflammatory cytokines","TGF-β, IL-10, IL-6","inhibition","Anti-inflammatory cytokines have the ability to inhibit the production of IL-1, TNF and other major pro-inflammatory cytokines and reduce T cell activation","(Flynn, 2004; Opal and DePalo, 2000)"]
["T cells","CD1-r T cells","differentiation","activation","The lipid antigen presenting molecule, CD1 stimulates a repertoire of unique CD1-restricted T cells.  These cells appear to go through processes of negative and positive selection in the thymus similar to MHC-restricted T cells.  Some CD1-restricted T cells have been found to possess the co-receptors CD4 or CD8, while other CD1-restricted T cells have been found to be double negative for the CD4 and CD8 co-receptors ","(Brigl and Brenner, 2004)"]
["CD1-r T cells","Apoptosis","perforin, granulysin","activation","The lysis of targets by CD8+ subset of CD1-restricted T cells depends on the release of granules containing perforin and granzymes","(Jullien et al, 1997)"]
["CD1-r T cells","Apoptosis","Fas-FasL interactions","activation","CD4- CD8- CD1-restricted T cells lyse targets through the Fas-FasL pathway","(Jullien et al, 1997)"]
["CD1-r T cells","T cells","IFN-γ","activation","This Th1 cytokine pattern can directly contribute to cell-mediated immunity against intracellular infection by enhancing T cell proliferation and macrophage activation","(Jullien et al, 1997)"]
["CD1-r T cells","Activated phagocytic cells","IFN-γ","activation","This Th1 cytokine pattern can directly contribute to cell-mediated immunity against intracellular infection by enhancing T cell proliferation and macrophage activation","(Jullien et al, 1997)"]
["Activated Dendritic Cells","CD1-r T cells","TCRs, MHCs, adhesion molecules","activation","The special role of DC in Ag presentation is underscored by their unique ability to present non-protein Ags to T cells via the non-classical MHC molecules CD1a, b, c","(Fortsch et al, 2000)"]

{"sheet":"References","index":1,"n_rows":35,"n_cols":1,"rows_kept":35,"cut":false,"hidden":false,"merged":[],"flags":["formulas_cached_only"]}
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