PMID- 15919369
OWN - NLM
STAT- MEDLINE
DCOM- 20050729
LR  - 20181201
IS  - 0008-8749 (Print)
IS  - 0008-8749 (Linking)
VI  - 231
IP  - 1-2
DP  - 2004 Sep-Oct
TI  - Differences in expression of cell surface co-stimulatory molecules, Toll-like 
      receptor genes and secretion of IL-12 by bone marrow-derived dendritic cells from 
      susceptible and resistant mouse strains in response to Coccidioides posadasii.
PG  - 49-55
AB  - Coccidioides posadasii is a soil fungus that causes coccidioidomycosis or Valley 
      Fever in the endemic regions of the southwestern US and Central America. Persons 
      with decreased T cells reactivity and immune deficiency are at increased risk of 
      developing severe disseminated infection. Among different mouse strains, DBA/2 
      mice are relatively resistant to C. posadasii whereas BALB/c mice are highly 
      susceptible, and this discrepancy has been attributed to the difference in the 
      development and expression of their Th1 cellular response. Dendritic cells (DC) 
      are the most potent antigen-presenting cells that are activated after taking up 
      pathogens or pathogens-derived antigens and regulate the immune response in the 
      host, including Th1 cellular response. However, the DC responses against C. 
      posadasii are not characterized. In the present study, we cultured bone-marrow 
      derived DC (BMDC) from BALB/c and DBA/2 mice and infected with C. posadasii 
      arthroconidia. The activation of BMDC was characterized by studying expression of 
      cell surface co-stimulatory molecules (CD11c, MHC class II, CD40, CD80, and 
      CD86), expression of genes encoding Toll-like receptors and release of IL-12. We 
      found that the BMDC from DBA/2 mice showed significant upregulation of Toll-like 
      receptor-2 and 4 genes expression, secretion of IL-12 (p<0.05) and modest 
      increase in T cell co-stimulatory molecules as compared to BMDC from BALB/c mice. 
      The data suggest that the differences in the activation status of DC in DBA/2 and 
      BALB/c mice may be responsible for the discrepancy in their susceptibility to C. 
      posadasii.
FAU - Awasthi, Shanjana
AU  - Awasthi S
AD  - Department of Pathology, University of Texas Health Science Center at San 
      Antonio, San Antonio, TX 78229, USA. awasthis@uthscsa.edu
FAU - Magee, D Mitchell
AU  - Magee DM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20041219
PL  - Netherlands
TA  - Cell Immunol
JT  - Cellular immunology
JID - 1246405
RN  - 0 (Receptors, Immunologic)
RN  - 0 (Tlr2 protein, mouse)
RN  - 0 (Tlr4 protein, mouse)
RN  - 0 (Toll-Like Receptor 2)
RN  - 0 (Toll-Like Receptor 4)
RN  - 187348-17-0 (Interleukin-12)
SB  - IM
MH  - Animals
MH  - Bone Marrow Cells/*cytology
MH  - Cell Differentiation
MH  - Cells, Cultured
MH  - Coccidioides/immunology/*physiology
MH  - Coccidioidomycosis/genetics/immunology/metabolism
MH  - Dendritic Cells/cytology/immunology/*metabolism
MH  - *Disease Susceptibility
MH  - Female
MH  - Gene Expression Regulation
MH  - Interleukin-12/*metabolism
MH  - Mice
MH  - Mice, Inbred DBA
MH  - Phenotype
MH  - Receptors, Immunologic/*genetics
MH  - Toll-Like Receptor 2
MH  - Toll-Like Receptor 4
EDAT- 2005/05/28 09:00
MHDA- 2005/07/30 09:00
CRDT- 2005/05/28 09:00
PHST- 2004/09/14 00:00 [received]
PHST- 2004/11/12 00:00 [revised]
PHST- 2004/11/16 00:00 [accepted]
PHST- 2005/05/28 09:00 [pubmed]
PHST- 2005/07/30 09:00 [medline]
PHST- 2005/05/28 09:00 [entrez]
AID - S0008-8749(04)00184-4 [pii]
AID - 10.1016/j.cellimm.2004.11.006 [doi]
PST - ppublish
SO  - Cell Immunol. 2004 Sep-Oct;231(1-2):49-55. doi: 10.1016/j.cellimm.2004.11.006. 
      Epub 2004 Dec 19.