Cytokines et Chimiokines
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Cytokines et Chimiokines
Actualités sur les cytokines et les chimiokines. Club de la SFI
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Club Cytokines et Chimiokines

The Colloque Cytokines et Chimiokines, is held every year since 1997 in the small resort town of Le Croisic at the Atlantic coast in Britanny. This meeting that gathers generally about one hundred participants is appreciated by reseachers and sponsors alike for its scientific content and its casual venue, as demonstrated by its 16 years of continued existence.

The themes of the 17th edition of the meeting deal with cytokines and the tumor environment, cytokines and immunometabolism, Intranuclear cytokines, biology and function of chemokine receptors. In addition to session "Cytokines and chemokines in the news", there wil be a special session on the biology of basophils.

Like the previous years, students and postdoctotal fellows are encouraged to present their work in a dedicated session.

The full program and details of the meeting are now on line.

Société Francaise d'Immunologie's insight:

pour plus d'informations

http://www.sfi-immunologie.com.fr/pages/?idl=21&page=619

 

Depuis 2012, le topic Scoop.it Immunology

http://www.scoop.it/t/immunology

inclut des posts dédiés aux cytokines.

Ont été inclus une quarantaine d'échantillons couvrant les thématiques abordées ci-dessus.

 

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16th TNF Superfamily Meeting | Australasian Society for Immunology |

16th TNF Superfamily Meeting | Australasian Society for Immunology | | Cytokines et Chimiokines | Scoop.it

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The Basophil-specific Protease mMCP-8 Provokes an Inflammatory Response in the Skin with Microvascular Hyperpermeability and Leukocyte Infiltration*

The Basophil-specific Protease mMCP-8 Provokes an Inflammatory Response in the Skin with Microvascular Hyperpermeability and Leukocyte Infiltration* | Cytokines et Chimiokines | Scoop.it
Basophils have often been erroneously considered to be minor relatives or blood-circulating precursors of tissue-resident mast cells because of some phenotypic similarity between them, including basophilic secretory granules in the cytoplasm. However, recent studies revealed that the repertoire of serine proteases stored in secretory granules is distinct in them. Particularly, mouse mast cell protease 8 (mMCP-8) is specifically expressed by basophils but not mast cells despite its name. Therefore, mMCP-8 is commonly used as a basophil-specific marker, but its functional property remains uncertain. Here we prepared recombinant mMCP-8 and examined its activity in vitro and in vivo. Purified recombinant mMCP-8 showed heat-sensitive proteolytic activity when α-tubulin was used as a substrate. One intradermal shot of mMCP-8, not heat-inactivated, induced cutaneous swelling with increased microvascular permeability in a cyclooxygenase-dependent manner. Moreover, repeated intradermal injection of mMCP-8 promoted skin infiltration of leukocytes, predominantly neutrophils and, to a lesser extent, monocytes and eosinophils, in conjunction with up-regulation of chemokine expression in the skin lesion. These results suggest that mMCP-8 is an important effector molecule in basophil-elicited inflammation, providing novel insights into how basophils exert a crucial and non-redundant role, distinct from that played by mast cells, in immune responses.
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IL-17 Blockade in Psoriasis

Publication date: 15 December 2016
Source:Cell, Volume 167, Issue 7
Author(s): Patrick R. Burkett, Vijay K. Kuchroo
IL-17A both directly induces and synergizes with other cytokines to promote autoimmune tissue inflammation. Secukinumab and ixekizumab are monoclonal antibodies (mAb) that inhibit interleukin-17A. These two agents were recently approved for treatment of psoriasis, and secukinumab is also approved for treatment of two spondyloarthropathies, psoriatic arthritis and ankylosing spondylitis.
Teaser IL-17A both directly induces and synergizes with other cytokines to promote autoimmune tissue inflammation. Secukinumab and ixekizumab are monoclonal antibodies (mAb) that inhibit interleukin-17A. These two agents were recently approved for treatment of psoriasis, and secukinumab is also approved for treatment of two spondyloarthropathies, psoriatic arthritis and ankylosing spondylitis.
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Device to treat sepsis wins first MIT Sloan Healthcare Innovations Prize | MIT Sloan School of Management

Device to treat sepsis wins first MIT Sloan Healthcare Innovations Prize | MIT Sloan School of Management | Cytokines et Chimiokines | Scoop.it
GoodSIRS takes $25,000 first prize; second prize to tanning bed with no UV radiation.
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Central Role of IL-23 and IL-17 Producing Eosinophils as Immunomodulatory Effector Cells in Acute Pulmonary Aspergillosis and Allergic Asthma. - PubMed - NCBI

Central Role of IL-23 and IL-17 Producing Eosinophils as Immunomodulatory Effector Cells in Acute Pulmonary Aspergillosis and Allergic Asthma. - PubMed - NCBI | Cytokines et Chimiokines | Scoop.it
PLoS Pathog. 2017 Jan 17;13(1):e1006175. doi: 10.1371/journal.ppat.1006175. [Epub ahead of print]
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IL-1beta and feeding

The deleterious effect of chronic activation of the IL-1β system on type 2 diabetes and other metabolic diseases is well documented. However, a possible physiological role for IL-1β in glucose metabolism has remained unexplored. Here we found that feeding induced a physiological increase in the number of peritoneal macrophages that secreted IL-1β, in a glucose-dependent manner. Subsequently, IL-1β contributed to the postprandial stimulation of insulin secretion. Accordingly, lack of endogenous IL-1β signaling in mice during refeeding and obesity diminished the concentration of insulin in plasma. IL-1β and insulin increased the uptake of glucose into macrophages, and insulin reinforced a pro-inflammatory pattern via the insulin receptor, glucose metabolism, production of reactive oxygen species, and secretion of IL-1β mediated by the NLRP3 inflammasome. Postprandial inflammation might be limited by normalization of glycemia, since it was prevented by inhibition of the sodium–glucose cotransporter SGLT2. Our findings identify a physiological role for IL-1β and insulin in the regulation of both metabolism and immunity.
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Mechanisms of immunomodulation by mammalian and viral decoy receptors: insights from structures

Immune responses are regulated by effector cytokines and chemokines that signal through cell surface receptors. Mammalian decoy receptors — which are typically soluble or inactive versions of cell surface receptors or soluble protein modules termed binding proteins — modulate and antagonize signalling by canonical effector–receptor complexes. Viruses have developed a diverse array of molecular decoys to evade host immune responses; these include viral homologues of host cytokines, chemokines and chemokine receptors; variants of host receptors with new functions; and novel decoy receptors that do not have host counterparts. Over the past decade, the number of known mammalian and viral decoy receptors has increased considerably, yet a comprehensive curation of the corresponding structure–mechanism relationships has not been carried out. In this Review, we provide a comprehensive resource on this topic with a view to better understanding the roles and evolutionary relationships of mammalian and viral decoy receptors, and the opportunities for leveraging their therapeutic potential.

Via Gilbert C FAURE
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Neutrophils releasing IL-17A into NETs are essential to plasma cell differentiation in inflamed tissue dependent on IL-1R. - PubMed - NCBI

Neutrophils releasing IL-17A into NETs are essential to plasma cell differentiation in inflamed tissue dependent on IL-1R. - PubMed - NCBI | Cytokines et Chimiokines | Scoop.it
Autoimmunity. 2016 Dec 23:1-16. doi: 10.1080/08916934.2016.1261834. [Epub ahead of print]
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JCI - The interferon paradox: can inhibiting an antiviral mechanism advance an HIV cure?

While antiretroviral therapy (ART) has improved the quality of life and increased the life span of many HIV-infected individuals, this therapeutic strategy has several limitations, including a lack of efficacy in fully restoring immune function and a requirement for life-long treatment. Two studies in this issue of the JCI use a humanized mouse model and demonstrate that type I interferon (IFN) is induced early during HIV infection and that type I IFN–associated gene signatures persist, even during ART. Importantly, blockade of type I IFN improved immune function, reduced the HIV reservoir, and caused a delay in viral rebound after ART interruption. Together, these two studies support further evaluation of IFN blockade as a supplement to ART.

Via Marcelo de Carvalho Bittencourt
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Interferon regulatory factor 2 protects mice from lethal viral neuroinvasion

Interferon regulatory factor 2 protects mice from lethal viral neuroinvasion | Cytokines et Chimiokines | Scoop.it
The host responds to virus infection by activating type I interferon (IFN) signaling leading to expression of IFN-stimulated genes (ISGs). Dysregulation of the IFN response results in inflammatory diseases and chronic infections. In this study, we demonstrate that IFN regulatory factor 2 (IRF2), an ISG and a negative regulator of IFN signaling, influences alphavirus neuroinvasion and pathogenesis. A Sindbis virus strain that in wild-type (WT) mice only causes disease when injected into the brain leads to lethal encephalitis in Irf2−/− mice after peripheral inoculation. Irf2−/− mice fail to control virus replication and recruit immune infiltrates into the brain. Reduced B cells and virus-specific IgG are observed in the Irf2−/− mouse brains despite the presence of peripheral neutralizing antibodies, suggesting a defect in B cell trafficking to the central nervous system (CNS). B cell–deficient μMT mice are significantly more susceptible to viral infection, yet WT B cells and serum are unable to rescue the Irf2−/− mice. Collectively, our data demonstrate that proper localization of B cells and local production of antibodies in the CNS are required for protection. The work advances our understanding of host mechanisms that affect viral neuroinvasion and their contribution to immunity against CNS infections.

Via Gilbert C FAURE
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Rheumatoid arthritis: Il-23 assists the transition from autoimmunity to inflammatory disease

Nature Reviews Rheumatology | doi:10.1038/nrrheum.2016.197
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Neutralizing anti-interleukin-1β antibodies reduce ischemia-related interleukin-1β transport across the blood–brain barrier in fetal sheep

Neutralizing anti-interleukin-1β antibodies reduce ischemia-related interleukin-1β transport across the blood–brain barrier in fetal sheep | Cytokines et Chimiokines | Scoop.it
Publication date: 27 March 2017
Source:Neuroscience, Volume 346
Author(s): Aparna Patra, Xiaodi Chen, Grazyna B. Sadowska, Jiyong Zhang, Yow-Pin Lim, James F. Padbury, William A. Banks, Barbara S. Stonestreet
Hypoxic ischemic insults predispose to perinatal brain injury. Pro-inflammatory cytokines are important in the evolution of this injury. Interleukin-1β (IL-1β) is a key mediator of inflammatory responses and elevated IL-1β levels in brain correlate with adverse neurodevelopmental outcomes after brain injury. Impaired blood–brain barrier (BBB) function represents an important component of hypoxic-ischemic brain injury in the fetus. In addition, ischemia–reperfusion increases cytokine transport across the BBB of the ovine fetus. Reducing pro-inflammatory cytokine entry into brain could represent a novel approach to attenuate ischemia-related brain injury. We hypothesized that infusions of neutralizing IL-1β monoclonal antibody (mAb) reduce IL-1β transport across the BBB after ischemia in the fetus. Fetal sheep were studied 24-h after 30-min of carotid artery occlusion. Fetuses were treated with placebo- or anti-IL-1β mAb intravenously 15-min and 4-h after ischemia. Ovine IL-1β protein expressed from IL-1β pGEX-2T vectors in Escherichia coli (E. coli) BL-21 cells was produced, purified, and radiolabeled with 125I. BBB permeability was quantified using the blood-to-brain transfer constant (Ki ) with 125I-radiolabeled-IL-1β. Increases in anti-IL-1β mAb were observed in the brain of the mAb-treated group (P <0.001). Blood-to-brain transport of 125I-IL-1β was lower (P <0.04) across brain regions in the anti-IL-1β mAb-treated than placebo-treated ischemic fetuses. Plasma 125I-IL-1β counts were higher (P <0.001) in the anti-IL-1β mAb- than placebo-treated ischemic fetuses. Systemic infusions of anti-IL-1β mAb reduce IL-1β transport across the BBB after ischemia in the ovine fetus. Our findings suggest that conditions associated with increases in systemic pro-inflammatory cytokines and neurodevelopmental impairment could benefit from an anti-cytokine therapeutic strategy.
Graphical abstract

Via Gilbert C FAURE
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A multichannel smartphone optical biosensor for high-throughput point-of-care diagnostics | InternetMedicine.com

A multichannel smartphone optical biosensor for high-throughput point-of-care diagnostics | InternetMedicine.com | Cytokines et Chimiokines | Scoop.it
Researchers develop portable smartphone spectrometer that they say can detect #Cancer with 99% accuracy https://t.co/P1UENNEzZq #TECS
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Sitagliptin inhibit human lymphocytes proliferation and Th1/Th17 differentiation in vitro

Sitagliptin inhibit human lymphocytes proliferation and Th1/Th17 differentiation in vitro | Cytokines et Chimiokines | Scoop.it
Publication date: 30 March 2017
Source:European Journal of Pharmaceutical Sciences, Volume 100
Author(s): Marcelo Maia Pinheiro, Caroline Lais Stoppa, Claudete Justina Valduga, Cristina Eunice Okuyama, Renata Gorjão, Regina Mara Silva Pereira, Susana Nogueira Diniz
Dipeptidyl peptidase-4 (DPP-4) inhibitors are a new class of anti-diabetic agents that are widely used in clinical practice to improve glycemic control in patients with type 2 diabetes. DPP-4 is also known as lymphocyte cell surface protein, CD26, and plays an important role in T-cell immunity. Recent studies suggest that DPP-4 inhibitors improve beta-cell function and attenuate autoimmunity in type 1 diabetic mouse models. To investigate the direct effect of DPP4 in immune response, human peripheral blood mononuclear cells (PBMC) from healthy volunteers were obtained by Ficoll gradient and cultivated in the absence (control) or presence of phytohemagglutinin (PHA), or stimulated with PHA and treated with sitagliptin. The immune modulation mechanisms analyzed were: cell proliferation, by MTT assay; cytokine quantification by ELISA or cytometric bead array (CBA), Th1/Th2/Th17 phenotyping by flow cytometric analysis and CD26 gene expression by real time PCR. The results showed that sitagliptin treatment inhibited the proliferation of PBMC-PHA stimulated cells in a dose dependent manner and decreased CD26 expression by these cells, suggesting that sitagliptin may interfere in CD26 expression, dimerization and cell signaling. Sitagliptin treatment not only inhibited IL-10 (p <0.05) and IFN-gamma (p =0.07) cytokines, but also completely abolish IL-6 expression by PBMCs (p <0.001). On the other hand, IL-4 were secreted in culture supernatants from sitagliptin treated cells. A statistically significant increase (p <0.05) in the ratio of TGF-beta/proliferation index after sitagliptin treatment (2627.97±1351.65), when comparing to untreated cells (646.28±376.94), was also demonstrated, indicating higher TGF-beta1 production by viable cells in cultures. Sitagliptin treatment induced a significantly (p <0.05) decrease in IL-17 and IFN-gamma intracellular expression compared with PHA alone. Also, the percentage of T CD4+ IL-17+, T CD4+ IFNgamma+ and T CD4+ IL-4+ cells were significantly reduced (p <0.05) by sitagliptin. Our data demonstrated an immunosuppressive effect of sitagliptin on Th1, Th17 and Th2 lymphocytes differentiation that leads to the generation of regulatory TGF-beta1 secreting cells with low CD26 gene expression that may influence the state of pancreatic beta-cells and controlling DM1 patients.
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Therapeutic Targeting of MLL Degradation Pathways in MLL-Rearranged Leukemia

Therapeutic Targeting of MLL Degradation Pathways in MLL-Rearranged Leukemia | Cytokines et Chimiokines | Scoop.it
Publication date: 12 January 2017
Source:Cell, Volume 168, Issues 1–2
Author(s): Kaiwei Liang, Andrew G. Volk, Jeffrey S. Haug, Stacy A. Marshall, Ashley R. Woodfin, Elizabeth T. Bartom, Joshua M. Gilmore, Laurence Florens, Michael P. Washburn, Kelly D. Sullivan, Joaquin M. Espinosa, Joseph Cannova, Jiwang Zhang, Edwin R. Smith, John D. Crispino, Ali Shilatifard
Chromosomal translocations of the mixed-lineage leukemia (MLL) gene with various partner genes result in aggressive leukemia with dismal outcomes. Despite similar expression at the mRNA level from the wild-type and chimeric MLL alleles, the chimeric protein is more stable. We report that UBE2O functions in regulating the stability of wild-type MLL in response to interleukin-1 signaling. Targeting wild-type MLL degradation impedes MLL leukemia cell proliferation, and it downregulates a specific group of target genes of the MLL chimeras and their oncogenic cofactor, the super elongation complex. Pharmacologically inhibiting this pathway substantially delays progression, and it improves survival of murine leukemia through stabilizing wild-type MLL protein, which displaces the MLL chimera from some of its target genes and, therefore, relieves the cellular oncogenic addiction to MLL chimeras. Stabilization of MLL provides us with a paradigm in the development of therapies for aggressive MLL leukemia and perhaps for other cancers caused by translocations.
Graphical abstract Teaser Stabilizing wild-type MLL proteins is a potential therapeutic approach for leukemia resulting from MLL translocations.
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CXCR3/CXCL10 Axis Regulates Neutrophil–NK Cell Cross-Talk Determining the Severity of Experimental Osteoarthritis

CXCR3/CXCL10 Axis Regulates Neutrophil–NK Cell Cross-Talk Determining the Severity of Experimental Osteoarthritis | Cytokines et Chimiokines | Scoop.it
Several immune cell populations are involved in cartilage damage, bone erosion, and resorption processes during osteoarthritis. The purpose of this study was to investigate the role of NK cells in the pathogenesis of experimental osteoarthritis and whether and how neutrophils can regulate their synovial localization in the disease. Experimental osteoarthritis was elicited by intra-articular injection of collagenase in wild type and Cxcr3 −/− 8-wk old mice. To follow osteoarthritis progression, cartilage damage, synovial thickening, and osteophyte formation were measured histologically. To characterize the inflammatory cells involved in osteoarthritis, synovial fluid was collected early after disease induction, and the cellular and cytokine content were quantified by flow cytometry and ELISA, respectively. We found that NK cells and neutrophils are among the first cells that accumulate in the synovium during osteoarthritis, both exerting a pathogenic role. Moreover, we uncovered a crucial role of the CXCL10/CXCR3 axis, with CXCL10 increasing in synovial fluids after injury and Cxcr3−/− mice being protected from disease development. Finally, in vivo depletion experiments showed that neutrophils are involved in an NK cell increase in the synovium, possibly by expressing CXCL10 in inflamed joints. Thus, neutrophils and NK cells act as important disease-promoting immune cells in experimental osteoarthritis and their functional interaction is promoted by the CXCL10/CXCR3 axis.
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Structural basis of ligand interaction with atypical chemokine receptor 3

Structural basis of ligand interaction with atypical chemokine receptor 3 | Cytokines et Chimiokines | Scoop.it
The atypical chemokine receptor 3 (ACKR3) is important for cell migration in development and cancer.
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IL-15 Activates the Jak3/STAT3 Signaling Pathway to Mediate Glucose Uptake in Skeletal Muscle Cells. - PubMed - NCBI

IL-15 Activates the Jak3/STAT3 Signaling Pathway to Mediate Glucose Uptake in Skeletal Muscle Cells. - PubMed - NCBI | Cytokines et Chimiokines | Scoop.it
Front Physiol. 2016 Dec 20;7:626. doi: 10.3389/fphys.2016.00626. eCollection 2016.
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IL1R9 Is Evolutionarily Related to IL18BP and May Function as an IL-18 Receptor


Via Gilbert C FAURE
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Blockade of CD47 ameliorates autoimmune inflammation in CNS by suppressing IL-1-triggered infiltration of pathogenic Th17 cells. - PubMed - NCBI

Blockade of CD47 ameliorates autoimmune inflammation in CNS by suppressing IL-1-triggered infiltration of pathogenic Th17 cells. - PubMed - NCBI | Cytokines et Chimiokines | Scoop.it
J Autoimmun. 2016 May;69:74-85. doi: 10.1016/j.jaut.2016.03.002. Epub 2016 Mar 16. Research Support, Non-U.S. Gov't

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Interleukin-12 bypasses common gamma-chain signalling in emergency natural killer cell lymphopoiesis

Interleukin-12 bypasses common gamma-chain signalling in emergency natural killer cell lymphopoiesis | Cytokines et Chimiokines | Scoop.it
Natural killer homeostasis is thought to be governed by gamma chain cytokines including IL-15.
Via Gilbert C FAURE
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Cutting Edge: LL-37–Mediated Formyl Peptide Receptor-2 Signaling in Follicular Dendritic Cells Contributes to B Cell Activation in Peyer’s Patch Germinal Centers

Peyer’s patches (PPs) are the major mucosal immune-inductive site, and germinal centers (GCs) in PPs determine the quality of the Abs produced. PP GCs are continuously induced by the gut microbiota, and their maintenance contributes to the induction of strong IgA responses to Ags. In this study, we investigated the role of formyl peptide receptor (FPR)-mediated signaling in the maintenance of PP GCs, because FPRs recognize the microbiota and initiate an innate immune response by chemotaxis. We found that follicular dendritic cells (FDCs), a key organizer of B cell follicles and GCs in mucosal immunity, express Fpr2. Additionally, Fpr2-mediated signaling in PP FDCs promoted Cxcl13 and B cell activating factor expression, as well as B cell proliferation and activation. Therefore, we suggest that Fpr2-mediated signaling in FDCs plays a key role in GC maintenance in PPs and results in an Ag-specific IgA response in the gut mucosal immune compartment.
Via Gilbert C FAURE
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Th2 Cells in Health and Disease. - PubMed - NCBI

Th2 Cells in Health and Disease. - PubMed - NCBI | Cytokines et Chimiokines | Scoop.it
Annu Rev Immunol. 2016 Nov 28. [Epub ahead of print]

Via Gilbert C FAURE
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T-Cell Immunophenotyping Distinguishes Active From Latent Tuberculosis

T-Cell Immunophenotyping Distinguishes Active From Latent Tuberculosis | Cytokines et Chimiokines | Scoop.it

Background. Changes in the phenotype and function of Mycobacterium tuberculosis (M. tuberculosis)-specific CD4[+] and CD8[+] T-cell subsets in response to stage of infection may allow discrimination between active tuberculosis and latent tuberculosis


Via Marcelo de Carvalho Bittencourt
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