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The Strathprints institutional repository is a digital archive of University of Strathclyde's Open Access research outputs. Strathprints provides access to thousands of Open Access research papers by University of Strathclyde researchers, including by researchers from the Department of Computer & Information Sciences involved in mathematically structured programming, similarity and metric search, computer security, software systems, combinatronics and digital health.

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An essential role for IL-13 in maintaining a non-healing response following leishmania mexicana infection

Alexander, James and Brombacher, Frank and McGachy, H.A. and McKenzie, A.N.J. and Walker, W. and Carter, K.C. (2002) An essential role for IL-13 in maintaining a non-healing response following leishmania mexicana infection. European Journal of Immunology, 32 (10). pp. 2923-2933. ISSN 0014-2980

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Abstract

A comparison of the growth of Leishmania mexicana in IL-4–/–, IL-4R–/– and wild-type BALB/c mice demonstrated a disease exacerbative role for IL-13 as well as IL-4. Thus, while both IL-4–/– and IL-4R–/– mice were more resistant than wild-type controls to infection with L. mexicana, IL-4R–/– mice, which are unresponsive to IL-13 as well as IL-4, were significantly more resistant to parasite growth than their IL-4–/– counterparts. Cytokine and antibody analysis revealed a Th1-biased specific response in both infected IL-4–/– and IL-4R–/– mice compared with wild-type animals. Reconstituting SCID mice with IL-4–/–, IL-4R–/– or wild-type splenocytes prior to infection demonstrated that the early onset of lesion growth was dependent on the presence of lymphocytes responding to IL-4 and/or IL-13, as lesions failed to develop in only the SCID IL-4R–/– reconstituted mice. An independent role for IL-13 in L. mexicana infection was demonstrated by comparing disease progression in IL-13–/–, IL-4–/–/IL-13–/– and wild-type B6/129 mice. In contrast to IL-4–/–/IL-13–/– mice, which were resistant, IL-13–/– mice developed lesions similar in size to wild-type animalsup to week 8 post infection. However, in contrast to wild-type mice in which disease continued to progress, lesions eventually healed in IL-13–/– mice, in association with the development of a Th1 response. Collectively our results suggest that IL-4 plays a critical role in early lesion development, and that IL-13 plays a crucial part in maintaining a chronic non-healing infection.