Maternal allergy influences the proliferation of neonatal T cells expressing CCR4, CXCR5 or CD103.
BACKGROUND
Elevated proliferative response to allergen in cord blood mononuclear cells (CBMCs) is related to subsequent allergy development of the neonate and has been suggested as a screening marker for high allergy risk.


OBJECTIVE
To characterize the proliferating cells in CBMCs from a neonatal group influenced by maternal allergy compared with a control group without known allergic heredity.


METHODS
CBMCs were stimulated with bovine beta-lactoglobulin (beta-LG) and proliferation was analysed by radioactive thymidine incorporation and expressed both as the traditional stimulation index (SI) and SI corrected by eliminating non-specific proliferation. After beta-LG combined with endotoxin stimulation, cellular expression of IL-4 and IFN-gamma mRNA was determined by quantitative RT-PCR and adhesion as well as chemokine receptors were analysed by three-colour flow cytometry in proliferating T cells (CD3+ Ki-67+).


RESULTS
The percentage of CCR4+ cells correlated weakly with concurrent IL-4 expression (r(S)=0.5, P<0.05), while CXCR3 correlated strongly with IFN-gamma expression (r(S)=0.83, P<0.001). In the allergy risk group, the percentage of proliferating T cells expressing CCR4 or integrin alphaE (CD103) was significantly reduced compared with the control group, while CXCR5 and the corrected SI were relatively increased (CCR4: P=0.01; integrin alphaE: P=0.03; CXCR5: P=0.04; SI: P=0.04).


CONCLUSIONS
Our results implied delayed maturation of immune functions involved in cellular migration, cell-cell interaction and immunoregulatory functions in neonates with hereditary allergy risk. The alterations observed in this subject group suggested that the corrected SI as well as proliferation of CCR4+, CXCR5+ or CD103+ T cells in allergen-stimulated CBMCs might serve as early screening markers for allergy risk.
Haddeland
U
U
Laboratory for Immunohistochemistry and Immunopathology (LIIPAT), Department and Institute of Pathology, University of Oslo, Rikshospitalet-Radiumhospitalet Medical Centre, Oslo, Norway.
Brandtzaeg
P
P
Nakstad
B
B
D000328:Adult; D000485:Allergens / Q000276:immunology / Q000494:pharmacology; D000818:Animals; D015703:Antigens, CD / Q000096:biosynthesis / Q000276:immunology*; D017252:CD3 Complex / Q000276:immunology; D002417:Cattle; D002450:Cell Communication / Q000187:drug effects / Q000276:immunology; D002465:Cell Movement / Q000187:drug effects / Q000276:immunology; D049109:Cell Proliferation / Q000187:drug effects; D004731:Endotoxins / Q000494:pharmacology; D005260:Female; D005312:Fetal Blood / Q000276:immunology* / Q000378:metabolism; D005434:Flow Cytometry; D005786:Gene Expression Regulation / Q000187:drug effects / Q000276:immunology; D006801:Humans; D006967:Hypersensitivity / Q000151:congenital / Q000209:etiology / Q000276:immunology* / Q000378:metabolism; D007231:Infant, Newborn; D039001:Integrin alpha Chains / Q000096:biosynthesis / Q000276:immunology*; D007371:Interferon-gamma / Q000276:immunology; D015847:Interleukin-4 / Q000276:immunology; D019394:Ki-67 Antigen / Q000276:immunology; D007782:Lactoglobulins / Q000276:immunology / Q000494:pharmacology; D008297:Male; D008431:Maternal-Fetal Exchange / Q000276:immunology*; D011247:Pregnancy; D054398:Receptors, CCR4; D054380:Receptors, CXCR5; D019707:Receptors, Chemokine / Q000096:biosynthesis / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology* / Q000378:metabolism
D000485:Allergens; D015703:Antigens, CD; C515354:CCR4 protein, human; D017252:CD3 Complex; C095085:CXCR5 protein, human; D004731:Endotoxins; C508598:IL4 protein, human; D039001:Integrin alpha Chains; D019394:Ki-67 Antigen; D007782:Lactoglobulins; D054398:Receptors, CCR4; D054380:Receptors, CXCR5; D019707:Receptors, Chemokine; C091367:alpha E integrins; D015847:Interleukin-4; D007371:Interferon-gamma