PMID- 18721326
OWN - NLM
STAT- MEDLINE
DCOM- 20080924
LR  - 20220318
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Print)
IS  - 0009-9104 (Linking)
VI  - 153 Suppl 1
IP  - Suppl 1
DP  - 2008 Sep
TI  - Allergy and the skin.
PG  - 27-9
LID - 10.1111/j.1365-2249.2008.03718.x [doi]
AB  - Allergic skin disorders include urticaria, angioedema, contact dermatitis and 
      atopic dermatitis, but the model fitting most closely the systemic concept of 
      allergy is atopic dermatitis (AD), the pathogenesis of which is linked to a 
      complex interaction between skin barrier dysfunction and environmental factors 
      such as allergens and microbes. In particular, an important advance was the 
      demonstration that the mutation of the skin barrier protein filaggrin is related 
      strictly to allergen sensitization and to the development of asthma in subjects 
      with AD. The altered skin barrier function, caused by several factors, results in 
      the passage of allergens through the skin and to systemic responses. A pivotal 
      role in such a response is exerted by Langerhans cells which, via their 
      immunoglobulin E (IgE) receptor, capture the allergens and present them to T 
      cells. When T helper type 2 (Th2) cells are activated, the production of a 
      proinflammatory cytokines and chemokines pattern sustains the persistence of 
      inflammation. Known AD-related cytokines are interleukin (IL)-5, IL-13 and tumour 
      necrosis factor (TNF)-alpha, with emerging importance for IL-17, which seems to 
      drive airway inflammation following cutaneous exposure to antigens, and IL-31, 
      which is expressed primarily in skin-homing Th2 cells. Skin-homing is another 
      crucial event in AD, mediated by the cutaneous lymphocyte-associated antigens 
      (CLA) receptor, which characterizes T cell subpopulations with different roles in 
      AD and asthma.
FAU - Incorvaia, C
AU  - Incorvaia C
AD  - Allergy/Pulmonary Rehabilitation Unit, ICP Hospital, Milan, Italy. 
      cristoforo.incorvaia@gmail.com
FAU - Frati, F
AU  - Frati F
FAU - Verna, N
AU  - Verna N
FAU - D'Alo, S
AU  - D'Alo S
FAU - Motolese, A
AU  - Motolese A
FAU - Pucci, S
AU  - Pucci S
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (Allergens)
RN  - 0 (Cytokines)
RN  - 0 (FLG protein, human)
RN  - 0 (Filaggrin Proteins)
RN  - 0 (Intermediate Filament Proteins)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Allergens/immunology
MH  - Animals
MH  - Cytokines/immunology
MH  - Dermatitis, Atopic/*immunology
MH  - Filaggrin Proteins
MH  - Humans
MH  - Hypersensitivity/*immunology
MH  - Immunoglobulin E/immunology
MH  - Intermediate Filament Proteins/metabolism
MH  - Langerhans Cells/immunology
MH  - Skin/*immunology
MH  - Th2 Cells/immunology
PMC - PMC2515356
EDAT- 2008/09/06 09:00
MHDA- 2008/09/25 09:00
PMCR- 2009/09/01
CRDT- 2008/09/06 09:00
PHST- 2008/09/06 09:00 [pubmed]
PHST- 2008/09/25 09:00 [medline]
PHST- 2008/09/06 09:00 [entrez]
PHST- 2009/09/01 00:00 [pmc-release]
AID - CEI3718 [pii]
AID - 10.1111/j.1365-2249.2008.03718.x [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2008 Sep;153 Suppl 1(Suppl 1):27-9. doi: 
      10.1111/j.1365-2249.2008.03718.x.