Publications
70 results found
Strid J, Hourihane J, Kimber I, et al., 2005, Epicutaneous exposure to peanut protein prevents oral tolerance and enhances allergic sensitization, CLINICAL AND EXPERIMENTAL ALLERGY, Vol: 35, Pages: 757-766, ISSN: 0954-7894
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- Citations: 178
de Noronha S, Hardy S, Sinclair J, et al., 2005, Impaired dendritic-cell homing in vivo in the absence of Wiskott-Aldrich syndrome protein, BLOOD, Vol: 105, Pages: 1590-1597, ISSN: 0006-4971
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- Citations: 88
Strid J, Thomson M, Hourihane J, et al., 2004, A novel model of sensitization and oral tolerance to peanut protein, IMMUNOLOGY, Vol: 113, Pages: 293-303, ISSN: 0019-2805
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- Citations: 92
Strid J, Hourihane J, Kimber I, et al., 2004, Disruption of the stratum corneum allows potent epicutaneous immunization with protein antigens resulting in a dominant systemic Th2 response, EUROPEAN JOURNAL OF IMMUNOLOGY, Vol: 34, Pages: 2100-2109, ISSN: 0014-2980
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Strid J, Hourihane J, Kimber I, et al., 2004, Disruption of the stratum corneum allows potent epicutaneous immunization with protein antigens resulting in a dominant systemic Th2 response., Eur J Immunol, Vol: 34, Pages: 2100-2109, ISSN: 0014-2980
The skin is an important immunological organ with an outer protective layer, the stratum corneum forming a barrier between the skin-associated lymphoid tissue and the environment. We show that gently removing the stratum corneum with adhesive tape permits potent epicutaneous immunization to protein antigens. IL-4 secretion by T cells from draining lymph nodes and high levels of specific IgE and IgG1 with no IgG2a showed that the immune responses induced following epicutaneous antigen exposure are strongly Th2 biased. Similar responses were obtained with different antigens and mouse strains. In contrast, subcutaneous immunization with antigen delivery into the dermis was less potent and gave predominantly Th1 responses. Removal of the stratum corneum increased expression of MHC class II, CD86, CD40, CD54 and CD11c on Langerhans cells, but did not cause them to migrate. Rapid migration from epidermis to draining lymph node was obtained, however, by exposure to antigen after removal of the stratum corneum, suggesting that maturation and migration of Langerhans cells are independently regulated events. These results suggest that antigen presentation by Langerhans cells gives predominantly Th2 responses. This may provide an explanation for allergic sensitization to some antigens. It may also be a useful non-invasive, non-adjuvant-dependent method of vaccination.
Strid J, Strobel S, 2002, The mucosal T cell, Food Allergy and Intolerance, Editors: Brostoff, Challacombe, Publisher: Saunders, Pages: 103-116
Strobel S, Strid J, 2002, Natural killer cells and aspects of intestinal immunity, Food Allergy and Intolerance, Editors: Brostoff, Challacombe, Publisher: Saunders, Pages: 117-126
Strid J, Lopes L, Marcinkiewicz J, et al., 2001, A defect in bone marrow derived dendritic cell maturation in the nonobesediabetic mouse, CLINICAL AND EXPERIMENTAL IMMUNOLOGY, Vol: 123, Pages: 375-381, ISSN: 0009-9104
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- Citations: 59
Lund T, Strid J, 2001, Is lack of peripheral tolerance induction a cause for diabetes in the non-obese diabetic mouse?, Autoimmunity, Editors: Górski, Krotkiewski, Zimecki, Publisher: Kluwer Academic Publishers, Pages: 139-160
Lund T, Strid J, 2000, Is lack of peripheral tolerance induction a cause for diabetes in the non-obese diabetic mouse?, Arch Immunol Ther Exp (Warsz), Vol: 48, Pages: 405-416, ISSN: 0004-069X
The non-obese diabetic (NOD) mouse is a spontaneous animal model for type 1 diabetes characterized by a selective destruction of the insulin producing beta cells in the pancreas. As in humans, the disease is controlled by several susceptibility genes, some of which map to the major histocompatibility complex on chromosome 17. However, environmental factors also contribute to the development of the disease in the NOD mouse, presumably through controlling the balance between the Th1 and Th2 response in the animal. Recent observations have shown that the NOD mouse has abnormalities in the development of bone marrow-derived antigen-presenting cells. These include the most potent activators of naive T cells, the dendritic cells, which exist in at least two different sub-populations; DC1 cells, responsible for activation of Th1 cells, and DC2 cells, which produce Th2 cells. In addition to activating naive T cells, the dendritic cells are also involved in generating central and peripheral tolerance to self molecules. In this process DC2 cells appear to be more important for the development of peripheral tolerance than DC1 cells. Besides abnormalities in the development of bone marrow-derived antigen-presenting cells, the NOD mouse also has a defect in the thymic selection of T cells, leading to a higher concentration of autoreactive T cells. We speculate that the NOD mouse may develop an imbalance in the two subsets of dendritic cells with a skewing towards DC cells, thus having a reduced ability to generate peripheral tolerance to a number of autoantigens.
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