PMID- 17118966
OWN - NLM
STAT- MEDLINE
DCOM- 20070525
LR  - 20220409
IS  - 0953-8178 (Print)
IS  - 0953-8178 (Linking)
VI  - 19
IP  - 1
DP  - 2007 Jan
TI  - Increased antigen presentation and T(h)1 polarization in genetically 
      histamine-free mice.
PG  - 51-8
AB  - Histamine is a well-known inflammatory mediator exerting various immunomodulatory 
      effects and affecting the development of antigen-specific immune responses. 
      Dendritic cells (DCs) are the most potent antigen-presenting cells specialized 
      for capture, uptake, transport, processing and presentation of antigens to T 
      cells. Using a genetically histamine-free [histidine decarboxylase knockout 
      (HDC-/-)] mouse model, we examined the effects of histamine on DC-mediated 
      antigen presentation. Applying an in vitro antigen presentation assay, we found 
      that spleen DCs, derived from HDC-/- mice, display a higher efficiency in antigen 
      presentation compared with wild-type cells. Flow cytometric characterization of 
      DCs disclosed that this difference was not due to an altered distribution of DCs 
      between or within the major functional sub-populations (assessed by CD11b and CD4 
      as myeloid and CD8alpha and DEC205 as lymphoid DC markers) or major changes in 
      the co-stimulatory molecule profile (CD40, CD80, CD86). However, real-time PCR 
      analysis of in vivo CFA-induced IL-12p35, IFNgamma, IL-10 and IL-4 expression 
      showed that DCs matured in a histamine-free environment exhibit significantly 
      elevated levels of IL-12p35 and IFNgamma mRNA. In vitro investigations confirmed 
      that isolated DCs, developed in the absence of histamine, exhibit indeed a 
      predominantly T(h)1-polarized cytokine pattern, as they show elevated levels of 
      IFNgamma mRNA upon LPS stimulation. Similar difference was found at the protein 
      level by ELISA, as well. Our study demonstrates that histamine interferes with 
      antigen presentation and alters the cytokine profile of DCs.
FAU - Jelinek, Ivett
AU  - Jelinek I
AD  - Department of Genetics, Cell and Immunobiology, Semmelweis University, Nagyvarad 
      ter 4, H-1089 Budapest, Hungary.
FAU - Laszlo, Valeria
AU  - Laszlo V
FAU - Buzas, Edit
AU  - Buzas E
FAU - Pallinger, Eva
AU  - Pallinger E
FAU - Hangya, Balazs
AU  - Hangya B
FAU - Horvath, Zsuzsanna
AU  - Horvath Z
FAU - Falus, Andras
AU  - Falus A
LA  - eng
PT  - Journal Article
DEP - 20061121
PL  - England
TA  - Int Immunol
JT  - International immunology
JID - 8916182
RN  - 0 (Antigens, CD)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-12 Subunit p35)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 820484N8I3 (Histamine)
RN  - 82115-62-6 (Interferon-gamma)
RN  - EC 4.1.1.22 (Histidine Decarboxylase)
SB  - IM
MH  - Animals
MH  - *Antigen Presentation/immunology
MH  - Antigens, CD/metabolism
MH  - Cytokines/metabolism
MH  - Dendritic Cells/drug effects/*immunology
MH  - Flow Cytometry
MH  - Histamine/physiology
MH  - Histidine Decarboxylase/*genetics
MH  - Interferon-gamma/genetics
MH  - Interleukin-12 Subunit p35/genetics
MH  - Lipopolysaccharides/pharmacology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Knockout
MH  - Polymerase Chain Reaction
MH  - RNA, Messenger/metabolism
MH  - Spleen/cytology
MH  - Th1 Cells/*immunology
EDAT- 2006/11/23 09:00
MHDA- 2007/05/26 09:00
CRDT- 2006/11/23 09:00
PHST- 2006/11/23 09:00 [pubmed]
PHST- 2007/05/26 09:00 [medline]
PHST- 2006/11/23 09:00 [entrez]
AID - dxl121 [pii]
AID - 10.1093/intimm/dxl121 [doi]
PST - ppublish
SO  - Int Immunol. 2007 Jan;19(1):51-8. doi: 10.1093/intimm/dxl121. Epub 2006 Nov 21.