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Fungi subvert vaccine T cell priming at the respiratory mucosa by preventing chemokine-induced influx of inflammatory monocytes.

Immunity | Apr 20, 2012

http://www.ncbi.nlm.nih.gov/pubmed/22483803

Vaccinologists strive to harness immunity at mucosal sites of pathogen entry. We studied respiratory delivery of an attenuated vaccine against Blastomyces dermatitidis. We created a T cell receptor transgenic mouse responsive to vaccine yeast and found that mucosal vaccination led to poor T cell activation in the draining nodes and differentiation in the lung. Mucosal vaccination subverted lung T cell priming by inducing matrix metalloproteinase 2 (MMP2), which impaired the action of the chemokine CCL7 on egress of CCR2(+) Ly6C(hi) inflammatory monocytes from the bone marrow and their recruitment to the lung. Studies in Mmp2(-/-) mice, or treatment with MMP inhibitor or rCCL7, restored recruitment of Ly6C(hi) monocytes to the lung and CD4(+) T cell priming. Mucosal vaccination against fungi and perhaps other respiratory pathogens may require manipulation of host MMPs in order to alter chemokine signals needed to recruit Ly6C(hi) monocytes and prime T cells at the respiratory mucosa.

Pubmed ID: 22483803 RIS Download

Mesh terms: Animals | Antigens, Ly | Blastomyces | Bone Marrow Cells | CD4-Positive T-Lymphocytes | Cell Differentiation | Cell Line | Cell Movement | Chemokine CCL7 | Fungal Vaccines | Inflammation | Lymphocyte Activation | Matrix Metalloproteinase 2 | Matrix Metalloproteinase Inhibitors | Mice | Mice, Transgenic | Monocytes | Respiratory Mucosa | Vaccination

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