scholarly journals Regulatory Effects of Macrophage Inflammatory Protein 1α/CCL3 on the Development of Immunity to Cryptococcus neoformans Depend on Expression of Early Inflammatory Cytokines

2001 ◽  
Vol 69 (10) ◽  
pp. 6256-6263 ◽  
Author(s):  
Michal A. Olszewski ◽  
Gary B. Huffnagle ◽  
Timothy R. Traynor ◽  
Roderick A. McDonald ◽  
Donald N. Cook ◽  
...  
Keyword(s):  
Cryptococcus Neoformans ◽  
Inflammatory Cytokines ◽  
Virulent Strain ◽  
Innate Immune ◽  
Necrosis Factor Alpha ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Ifn Γ ◽  
The Brain ◽  
Macrophage Inflammatory Protein

ABSTRACT Macrophage inflammatory protein 1α (MIP-1α)/CCL3 prevents the development of eosinophilic pneumonia (EP) driven by a nonprotective T2-type immunity during infection with a highly virulent strain ofCryptococcus neoformans. The present study evaluated the interaction of MIP-1α with other innate immune system cytokines by comparing the immune responses that followed pulmonary infections with high- (C. neoformans 145A) and low (C. neoformans 52D)-virulence strains. In contrast to what was found for C. neoformans 145A infection, lack of MIP-1α in C. neoformans 52D infection did not cause the development of EP. C. neoformans 52D induced tumor necrosis factor alpha (TNF-α), gamma interferon (IFN-γ), and MCP-1 in the lungs of infected wild-type (WT) and MIP-1α knockout (KO) mice by day 7 postinfection. Both WT and MIP-1α KO mice subsequently cleared this infection. Thus, the robust expression of early inflammatory cytokines in C. neoformans 52D-infected mice promoted the development of protective immunity even in the absence of MIP-1α. Alternatively, C. neoformans145A-infected WT and MIP-1α KO mice had diminished TNF-α, IFN-γ, and macrophage chemoattractant protein 1 (MCP-1) responses, indicating that virulent C. neoformans 145A evaded early innate host defenses. However C. neoformans145A-infected WT mice had an early induction of MIP-1α and subsequently did not develop EP. In contrast, C. neoformans 145A-infected MIP-1α KO mice developed EP and had increased C. neoformans dissemination into the brain by day 35. We conclude that, in the absence of other innate immune response effector molecules, MIP-1α is crucial to prevent the development of EP and to control C. neoformansdissemination to the brain.

scholarly journals Simultaneous Measurement of Antigen-Stimulated Interleukin-1β and Gamma Interferon Production Enhances Test Sensitivity for the Detection of Mycobacterium bovis Infection in Cattle

2010 ◽  
Vol 17 (12) ◽  
pp. 1946-1951 ◽  
Author(s):  
Gareth J. Jones ◽  
Chris Pirson ◽  
R. Glyn Hewinson ◽  
H. Martin Vordermeier
Keyword(s):  
Mycobacterium Bovis ◽  
Gamma Interferon ◽  
Interleukin 1Β ◽  
Induced Responses ◽  
Readout System ◽  
Necrosis Factor Alpha ◽  
Test Sensitivity ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Ifn Γ

ABSTRACT In order to identify cytokines that may be useful as candidates for inclusion in diagnostic tests for Mycobacterium bovis infection in cattle, we compared the levels of gamma interferon (IFN-γ), interleukin 1β (IL-1β), IL-4, IL-10, IL-12, macrophage inflammatory protein 1β (MIP-1β), and tumor necrosis factor alpha (TNF-α) in whole-blood cultures from tuberculosis (TB) reactor animals or TB-free controls following stimulation with M. bovis-specific antigens (purified protein derivative from M. bovis [PPD-B] or ESAT-6/CFP-10). In addition to IFN-γ responses, the production of IL-1β and TNF-α was also statistically significantly elevated in TB reactor cattle over that in uninfected controls following stimulation with PPD-B or ESAT-6/CFP-10 peptides. Thus, we evaluated whether the use of these two additional readouts could disclose further animals not detected by measuring IFN-γ alone. To this end, receiver operating characteristic (ROC) analyses were performed to define diagnostic cutoffs for positivity for TNF-α and IL-1β. These results revealed that for ESAT-6/CFP-10-induced responses, the use of all three readouts (IFN-γ, TNF-α, and IL-1β) in parallel increased the sensitivity of detection of M. bovis-infected animals by 11% but also resulted in a specificity decrease of 14%. However, applying only IFN-γ and IL-1β in parallel resulted in a 5% increase in sensitivity without the corresponding loss of specificity. The results for PPD-B-induced responses were similar, although the loss of specificity was more pronounced, even when only IFN-γ and IL-1β were used as readout systems. In conclusion, we have demonstrated that the use of an additional readout system, such as IL-1β, can potentially complement IFN-γ by increasing overall test sensitivity for the detection of M. bovis infection in cattle.

scholarly journals Gene Expression and Production of Tumor Necrosis Factor Alpha, Interleukin-1β (IL-1β), IL-8, Macrophage Inflammatory Protein 1α (MIP-1α), MIP-1β, and Gamma Interferon-Inducible Protein 10 by Human Neutrophils Stimulated with Group B Meningococcal Outer Membrane Vesicles

2000 ◽  
Vol 68 (12) ◽  
pp. 6917-6923 ◽  
Author(s):  
José A. Lapinet ◽  
Patrizia Scapini ◽  
Federica Calzetti ◽  
Oliver Pérez ◽  
Marco A. Cassatella
Keyword(s):  
Membrane Vesicles ◽  
Outer Membrane Vesicles ◽  
Necrosis Factor Alpha ◽  
Cytokines And Chemokines ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Factor Alpha ◽  
Ifn Γ ◽  
Inducible Protein ◽  
Necrosis Factor

ABSTRACT Accumulation of polymorphonuclear neutrophils (PMN) into the subarachnoidal space is one of the hallmarks of Neisseria meningitidis infection. In this study, we evaluated the ability of outer membrane vesicles (OMV) from N. meningitidis B to stimulate cytokine production by neutrophils. We found that PMN stimulated in vitro by OMV produce proinflammatory cytokines and chemokines including tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), IL-8, macrophage inflammatory protein 1α (MIP-1α), and MIP-1β. A considerable induction of gamma interferon (IFN-γ)-inducible protein 10 (IP-10) mRNA transcripts, as well as extracellular IP-10 release, was also observed when neutrophils were stimulated by OMV in combination with IFN-γ. Furthermore, PMN stimulated by OMV in the presence of IFN-γ demonstrated an enhanced capacity to release TNF-α, IL-1β, IL-8, and MIP-1β compared to stimulation with OMV alone. In line with its downregulatory effects on neutrophil-derived proinflammatory cytokines, IL-10 potently inhibited TNF-α, IL-1β, IL-8, and MIP-1β production triggered by OMV. Finally, a neutralizing anti-TNF-α monoclonal antibody (MAb) did not influence the release of IL-8 and MIP-1β induced by OMV, therefore excluding a role for endogenous TNF-α in mediating the induction of chemokine release by OMV. In contrast, the ability of lipopolysaccharide fromN. meningitidis B to induce the production of IL-8 and MIP-1β was significantly inhibited by anti-TNF-α MAb. Our results establish that, in response to OMV, neutrophils produce a proinflammatory profile of cytokines and chemokines which may not only play a role in the pathogenesis of meningitis but may also contribute to the development of protective immunity to serogroup B meningococci.

scholarly journals Suppression of Macrophage Activation with CNI-1493 Increases Survival in Infant Rats with Systemic Haemophilus influenzae Infection

2000 ◽  
Vol 68 (9) ◽  
pp. 5329-5334 ◽  
Author(s):  
Carl Granert ◽  
Hana Abdalla ◽  
Lars Lindquist ◽  
Asim Diab ◽  
Moiz Bakhiet ◽  
...  
Keyword(s):  
Haemophilus Influenzae ◽  
Interleukin 1 ◽  
Necrosis Factor Alpha ◽  
Infant Rats ◽  
Cytokine Inhibition ◽  
Tnf Α ◽  
Factor Alpha ◽  
Ifn Γ ◽  
The Brain ◽  
Necrosis Factor

ABSTRACT CNI-1493, a potent macrophage deactivator, was used to treat infant rats systemically infected with Haemophilus influenzae type b (Hib). CNI-1493 was injected 1 h prior to bacterial inoculation and 24 h later and resulted in a 75 percent increased rate of survival compared to that for untreated controls. The effect of CNI-1493 on the inflammatory response was studied by immunohistochemical detection of individual tumor necrosis factor alpha (TNF-α)-, interleukin 1 beta (IL-1β)-, and gamma interferon (IFN-γ)-producing cells in the spleen. A significant reduction of the incidence of TNF-α- and IL-1β-expressing cells was found for CNI-1493-treated animals. IFN-γ expression was not suppressed by CNI-1493, indicating that cytokine inhibition was specific in macrophages. CNI-1493 significantly reduced the number of infiltrating granulocytes in the brain from that for controls. This study provides evidence that CNI-1493 protects against lethal Hib infection by deactivating the inflammatory cascade in infant rats.

scholarly journals Haemophilus influenzae Porin Contributes to Signaling of the Inflammatory Cascade in Rat Brain

2001 ◽  
Vol 69 (1) ◽  
pp. 221-227 ◽  
Author(s):  
Massimiliano Galdiero ◽  
Michele D'Amico ◽  
Fernanda Gorga ◽  
Clara Di Filippo ◽  
Marina D'Isanto ◽  
...  
Keyword(s):  
Haemophilus Influenzae ◽  
Serum Proteins ◽  
Necrosis Factor Alpha ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Factor Alpha ◽  
Interleukin 1Α ◽  
Macrophage Inflammatory Protein ◽  
Brain Water ◽  
Necrosis Factor

ABSTRACT In the present study we observed that the Haemophilus influenzae type b (Hib) porin, among the different surface bacterial components, is involved in the pathophysiology of bacterial meningitis. This study demonstrates that inoculation of Hib porin into the fourth cerebral ventricle causes the simultaneous expression of interleukin-1α (IL-1α), tumor necrosis factor alpha (TNF-α), and macrophage inflammatory protein 2 (MIP-2) at 6 h after inoculation. At 24 h, the expression of MIP-2 decreases while the expression of IL-1α and TNF-α increases. The mRNA expression of IL-1α, TNF-α, and MIP-2 is correlated with injury to the blood-brain barrier as demonstrated by the appearance of serum proteins and leukocytes in cerebrospinal fluid and by the increase in brain water content.

scholarly journals CCL20/Macrophage Inflammatory Protein 3α and Tumor Necrosis Factor Alpha Production by Primary Uterine Epithelial Cells in Response to Treatment with Lipopolysaccharide or Pam3Cys

2005 ◽  
Vol 73 (1) ◽  
pp. 476-484 ◽  
Author(s):  
Mardi A. Crane-Godreau ◽  
Charles R. Wira
Keyword(s):  
Tumor Necrosis Factor ◽  
Epithelial Cells ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Factor Alpha ◽  
Macrophage Inflammatory Protein ◽  
Necrosis Factor

ABSTRACT Having previously shown that CCL20/macrophage inflammatory protein 3α and tumor necrosis factor alpha (TNF-α) are released by polarized primary rat uterine epithelial cells (UEC) in response to Escherichia coli but not to Lactobacillus rhamnosus, we sought to determine if epithelial cells are responsive to pathogen-associated molecular patterns (PAMP), including lipopolysaccharide (LPS), lipoteichoic acid (LTA), and Pam3Cys, a bacterial lipoprotein analog. Epithelial cells were grown to confluence on Nunc cell culture inserts prior to apical treatment with PAMPs. In response to LPS, LTA, and Pam3Cys (EMC Microcollection GmbH, Tübingen, Germany), CCL20 levels increased (4- to 10-fold) while PAMPs caused increased TNF-α (1- to 4-fold) in the medium collected after 24 h of incubation. Both apical and basolateral secretion of CCL20 and TNF-α increased in response to PAMPs, but treatments had no effect on cell viability and integrity, as measured by transepithelial resistance. Time course studies of CCL20 and TNF-α release in response to Pam3Cys and LPS indicated that CCL20 release peaked between 2 and 4 h after treatment, whereas TNF-α release was gradual over the length of the incubation. Freeze-thaw and cell lysis experiments, along with actinomycin D studies, suggested that CCL20 and TNF-α are synthesized in response to PAMP stimulation. Taken together, these studies demonstrate that E. coli and selected PAMPs have direct effects on the production of CCL20 and TNF-α without affecting cell integrity. Since CCL20 is known to be both chemotactic and antimicrobial, the increase in apical and basolateral release by UEC in response to PAMPs suggests a new mechanism of innate immune protection in the female reproductive tract.

scholarly journals Enhanced Innate Immune Responsiveness to Pulmonary Cryptococcus neoformans Infection Is Associated with Resistance to Progressive Infection

2008 ◽  
Vol 76 (10) ◽  
pp. 4745-4756 ◽  
Author(s):  
Loïc Guillot ◽  
Scott F. Carroll ◽  
Robert Homer ◽  
Salman T. Qureshi
Keyword(s):  
Immune Response ◽  
Cryptococcus Neoformans ◽  
Innate Immune Response ◽  
Intracellular Signaling ◽  
Inbred Mouse ◽  
Inbred Mouse Strain ◽  
Innate Immune ◽  
Natural Resistance ◽  
Necrosis Factor Alpha ◽  
Tnf Α

ABSTRACT Genetically regulated mechanisms of host defense against Cryptococcus neoformans infection are not well understood. In this study, pulmonary infection with the moderately virulent C. neoformans strain 24067 was used to compare the host resistance phenotype of C57BL/6J with that of inbred mouse strain SJL/J. At 7 days or later after infection, C57BL/6J mice exhibited a significantly greater fungal burden in the lungs than SJL/J mice. Characterization of the pulmonary innate immune response at 3 h after cryptococcal infection revealed that resistant SJL/J mice exhibited significantly higher neutrophilia, with elevated levels of inflammatory cytokine tumor necrosis factor alpha (TNF-α) and keratinocyte-derived chemokine (KC)/CXCL1 in the airways, as well as increased whole-lung mRNA expression of chemokines KC/CXCL1, MIP-1α/CCL3, MIP-1β/CCL4, MIP-2/CXCL2, and MCP-1/CCL2 and cytokines interleukin 1β (IL-1β) and IL-1Ra. At 7 and 14 days after infection, SJL/J mice maintained significantly higher levels of TNF-α and KC/CXCL1 in the airways and exhibited a Th1 response characterized by elevated levels of lung gamma interferon (IFN-γ) and IL-12/IL-23p40, while C57BL/6J mice exhibited Th2 immunity as defined by eosinophilia and IL-4 production. Alveolar and resident peritoneal macrophages from SJL/J mice also secreted significantly greater amounts of TNF-α and KC/CXCL1 following in vitro stimulation with C. neoformans. Intracellular signaling analysis demonstrated that TNF-α and KC/CXCL1 production was regulated by NF-κB and phosphatidylinositol 3 kinase in both strains; however, SJL/J macrophages exhibited heightened and prolonged activation in response to C. neoformans infection compared to that of C57BL/6J. Taken together, these data demonstrate that an enhanced innate immune response against pulmonary C. neoformans infection in SJL/J mice is associated with natural resistance to progressive infection.

scholarly journals Effects of Estradiol on Lipopolysaccharide and Pam3Cys Stimulation of CCL20/Macrophage Inflammatory Protein 3 Alpha and Tumor Necrosis Factor Alpha Production by Uterine Epithelial Cells in Culture

2005 ◽  
Vol 73 (7) ◽  
pp. 4231-4237 ◽  
Author(s):  
Mardi A. Crane-Godreau ◽  
Charles R. Wira
Keyword(s):  
Tumor Necrosis Factor ◽  
Epithelial Cells ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Ici 182,780 ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Factor Alpha ◽  
Macrophage Inflammatory Protein ◽  
Necrosis Factor

ABSTRACT We have previously demonstrated that rat uterine epithelial cells (UEC) produce CCL20/macrophage inflammatory protein 3 alpha (MIP3α) and tumor necrosis factor alpha (TNF-α) in response to live and heat-killed Escherichia coli and to the pathogen-associated molecular patterns (PAMP) lipopolysaccharide (LPS) and Pam3Cys. To determine whether estradiol (E2) modulates PAMP-induced CCL20/MIP3α and TNF-α secretion, primary cultures of rat UEC were incubated with E2 for 24 h and then treated with LPS or Pam3Cys or not treated for an additional 12 h. E2 inhibited the constitutive secretion of TNF-α and CCL20/MIP3α into culture media. Interestingly, E2 pretreatment enhanced CCL20/MIP3α secretion due to LPS and Pam3Cys administration. In contrast, and at the same time, E2 lowered the TNF-α response to both PAMP. To determine whether estrogen receptors (ER) mediated the effects of E2, epithelial cells were incubated with E2 and/or ICI 182,780, a known ER antagonist. ICI 182,780 had no effect on E2 inhibition of constitutive TNF-α and CCL20/MIP3α secretion. In contrast, ICI 182,780 reversed the stimulatory effect of E2 on LPS- and/or Pam3Cys-induced CCL20/MIP3α secretion as well as partially reversed the inhibitory effect of E2 on TNF-α production by epithelial cells. Overall, these results indicate that E2 regulates the production of TNF-α and CCL20/MIP3α by UEC in the absence as well as presence of PAMP. Since CCL20/MIP3α has antimicrobial activity and is chemotactic for immune cells, these studies suggest that regulation of CCL20/MIP3α and TNF-α by E2 and PAMP may have profound effects on innate and adaptive immune responses to microbial challenge in the female reproductive tract.

Time course of cytokine, corticosterone, and tissue injury responses in mice during heat strain recovery

2006 ◽  
Vol 100 (4) ◽  
pp. 1400-1409 ◽  
Author(s):  
Lisa R. Leon ◽  
Michael D. Blaha ◽  
David A. DuBose
Keyword(s):  
Core Temperature ◽  
Time Course ◽  
Tissue Injury ◽  
Heat Strain ◽  
Strain Recovery ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Cytokine Milieu ◽  
Ifn Γ ◽  
Macrophage Inflammatory Protein

Elevated circulating cytokines are observed in heatstroke patients, suggesting a role for these substances in the pathophysiological responses of this syndrome. Typically, cytokines are determined at end-stage heatstroke such that changes throughout progression of the syndrome are poorly understood. We hypothesized that the cytokine milieu changes during heatstroke progression, correlating with thermoregulatory, hemodynamic, and tissue injury responses to heat exposure in the mouse. We determined plasma IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, IL-12p40, IL-12p70, IFN-γ, macrophage inflammatory protein-1α, TNF-α, corticosterone, glucose, hematocrit, and tissue injury during 24 h of recovery. Mice were exposed to ambient temperature of 39.5 ± 0.2°C, without food and water, until maximum core temperature (Tc,Max) of 42.7°C was attained. During recovery, mice displayed hypothermia (29.3 ± 0.4°C) and a feverlike elevation at 24 h (control = 36.2 ± 0.3°C vs. heat stressed = 37.8 ± 0.3°C). Dehydration (∼10%) and hypoglycemia (∼65–75% reduction) occurred from Tc,Max to hypothermia. IL-1α, IL-2, IL-4, IL-12p70, IFN-γ, TNF-α, and macrophage inflammatory protein-1α were undetectable. IL-12p40 was elevated at Tc,Max, whereas IL-1β, IL-6, and IL-10 inversely correlated with core temperature, showing maximum production at hypothermia. IL-6 was elevated, whereas IL-12p40 levels were decreased below baseline at 24 h. Corticosterone positively correlated with IL-6, increasing from Tc,Max to hypothermia, with recovery to baseline by 24 h. Tissue lesions were observed in duodenum, spleen, and kidney at Tc,Max, hypothermia, and 24 h, respectively. These data suggest that the cytokine milieu changes during heat strain recovery with similarities between findings in mice and those described for human heatstroke, supporting the application of our model to the study of cytokine responses in vivo.

scholarly journals Inflammatory Cytokines Enhance the Interaction of Mannheimia haemolytica Leukotoxin with Bovine Peripheral Blood Neutrophils In Vitro

2002 ◽  
Vol 70 (8) ◽  
pp. 4336-4343 ◽  
Author(s):  
F. Leite ◽  
S. O'Brien ◽  
M. J. Sylte ◽  
T. Page ◽  
D. Atapattu ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Peripheral Blood ◽  
Biological Response ◽  
Lymphocyte Function ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Blood Neutrophils ◽  
Ifn Γ ◽  
Bovine Pneumonic Pasteurellosis

ABSTRACT Mannheimia (Pasteurella) haemolytica A1 produces several virulence factors that play an important role in the pathogenesis of bovine pneumonic pasteurellosis. Foremost among these is a leukotoxin (LKT) that specifically kills ruminant leukocytes. Recent evidence suggests that M. haemolytica LKT binding to bovine leukocytes is mediated by the β2-integrin CD11a/CD18 (lymphocyte function-associated antigen 1 [LFA-1]), which subsequently induces activation and cytolysis of these cells. Inflammatory cytokines, which are released during viral and bacterial infection, are reported to increase LFA-1 expression and conformational activation. We investigated the effects of the inflammatory cytokines interleukin-1β (IL-1β), tumor necrosis factor alpha (TNF-α), and gamma interferon (IFN-γ) on the interaction of M. haemolytica LKT with bovine peripheral blood neutrophils (PMNs). In this study we demonstrated, by flow cytometry, that bovine PMNs increased their binding to an anti-bovine LFA-1 monoclonal antibody (BAT75A) following in vitro incubation with IL-1β, TNF-α, or IFN-γ. Incubation with cytokines also increased CD18 expression, as assessed by real-time PCR and by Western blotting. Increased LFA-1 expression by PMNs exposed to cytokines was associated with increased LKT binding and cytotoxicity. The latter represented, at least in part, enhanced PMN apoptosis, as assessed by propidium iodine staining and caspase-3 activation. The results of this study suggest that inflammatory cytokines may play an important role in enhancing the biological response of bovine PMNs to M. haemolytica LKT.

scholarly journals Antibody-Mediated Protection against Cryptococcus neoformans Pulmonary Infection Is Dependent on B Cells

2005 ◽  
Vol 73 (2) ◽  
pp. 1141-1150 ◽  
Author(s):  
Johanna Rivera ◽  
Oscar Zaragoza ◽  
Arturo Casadevall
Keyword(s):  
B Cells ◽  
B Cell ◽  
Cryptococcus Neoformans ◽  
Scid Mice ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Inflammatory Protein ◽  
Ifn Γ ◽  
Macrophage Inflammatory Protein ◽  
Deficient Mice

ABSTRACT The pathogenesis of pulmonary Cryptococcus neoformans infection and the efficacy of passive immunoglobulin G1 (IgG1) administration were investigated in B-cell-deficient and C57BL/6J mice. C57BL/6J mice lived longer than B-cell-deficient mice after both intratracheal and intravenous infections. Administration of IgG1 prior to infection prolonged the survival of C57BL/6J mice but had no effect on the survival or numbers of CFU in the lungs of B-cell-deficient mice. C. neoformans infection in B-cell-deficient mice resulted in significantly higher levels of gamma interferon (IFN-γ), monocyte chemoattractant protein-1 (MCP-1), and macrophage inflammatory protein-1α (MIP-1α) than in C57BL/6J mice. IgG1 administration reduced IFN-γ and MCP-1 levels in C57BL/6J mice but not in B-cell-deficient mice. In addition, compared to its effect in C57BL/6J mice, C. neoformans infection in FcRγIII-deficient, athymic, and SCID mice significantly increased IFN-γ and MCP-1 levels. IgG1 administration was associated with reduced IFN-γ levels in C57BL/6J mice but not in FcRγIII-deficient, athymic, and SCID mice. These observations suggest that IgG1-mediated protection in this system is a consequence of alterations in the inflammatory response that translate into less damage to the host without directly reducing the fungal burden. For hosts with impaired immunities, the ineffectiveness of passive antibody (Ab) may reflect an inability to down-regulate inflammation and avoid self-damage. The results indicate an important role for B cells in host defense against C. neoformans infection and demonstrate a surprising dependence of Ab-mediated protection on B cells in this system.

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