Blood vessels in human immunodeficiency virus‐related lymphadenopathy: high endothelial venules and lymphocyte migration

Csanaky, G; T, Pap; Kalász, Veronika; Kelényi, G

doi:10.1111/j.1699-0463.1991.tb01239.x

Cited by 2 publications

(1 citation statement)

References 13 publications

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“…These results indicated that the increased input of naïve lymphocytes to the dLN is at least in part mediated by a rapid increase in the number of HEVs. We reasoned that the increase in lymphocyte recruitment through additional HEVs must be achieved by an increase in blood supply into the LNs, as suggested by previous studies in larger animals (24,29,30). If so, the arteriole feeding the dLN must expand to accommodate an increase in blood flow.…”

Section: Mechanism Of Inflammation-induced Recirculationmentioning

confidence: 85%

Innate control of adaptive immunity via remodeling of lymph node feed arteriole

Soderberg

Payne

Sato

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

136

159

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The adaptive immune system relies on rare cognate lymphocytes to detect pathogen-derived antigens. Naïve lymphocytes recirculate through secondary lymphoid organs in search of cognate antigen. Here, we show that the naïve-lymphocyte recirculation pattern is controlled at the level of innate immune recognition, independent of antigen-specific stimulation. We demonstrate that inflammation-induced lymphocyte recruitment to the lymph node is mediated by the remodeling of the primary feed arteriole, and that its physiological role is to increase the efficiency of screening for rare antigen-specific lymphocytes. Our data reveal a mechanism of innate control of adaptive immunity: by increasing the pool of naïve lymphocytes for detection of foreign antigens via regulation of vascular input to the local lymph node.

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Section: Mechanism Of Inflammation-induced Recirculationmentioning

confidence: 85%

Innate control of adaptive immunity via remodeling of lymph node feed arteriole

Soderberg

Payne

Sato

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

136

159

View full text Add to dashboard Cite

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Function of CD4+CD3− cells in relation to B- and T-zone stroma in spleen

Kim

McConnell

Gaspal

et al. 2006

Blood

103

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Lymphocytes from lymphotoxin (LT)␣ IntroductionThe development of segregated B-cell and T-cell areas within secondary lymphoid organs is the platform for the development of both high-affinity class-switched antibodies and memory antibody responses; neither of these functions develops in lymphotoxin (LT) ␣ Ϫ/Ϫ mice, in which there is no B/T segregation. 1 The absence of segregation is due to impaired organization rather than intrinsic defects in the lymphocytes themselves, as LT␣ Ϫ/Ϫ lymphocytes both segregate and function normally following transfer into irradiated normal 2 or RAG-deficient 1 hosts, which lack B and T cells. A cellular source other than mature B or T cells is therefore implicated in the process of organization.LT␤R signals and perhaps TNFR1 signals mediate lymphoid B/T segregation by activating subpopulations of stromal cells, which then switch on the expression of chemokine genes. 3 The expression of CCR7 ligand attracts dendritic cells (DCs) and T cells to form the T-cell area 4 ; the expression of CXCR5 ligand brings B cells together to form follicles. 5 The genes for these receptors, TNFR1 and LT␤R, are tightly linked on chromosome 12 in humans and chromosome 6 in mice, implying that they arose by local gene duplication prior to speciation of human and mouse.The expression of the T-zone chemokines in lymph nodes is normal in RAG Ϫ/Ϫ mice, although the expression of the B-zone chemokine, CXCL13, is reduced to approximately 20%, and normal expression depends on B cells. 6 Along with the LT␣ Ϫ/Ϫ lymphocyte transfer experiments, these data suggest that there is a non-B non-T cell capable of inducing normal (T zone) and partial (B zone) chemokine expression in stroma.In this paper, we extend previous observations demonstrating a role for a non-B non-T cell in B/T segregation, 2 and identify CD4 ϩ CD3 Ϫ cells that we have previously implicated in T-cell memory for antibody responses in adult mice 7,8 as playing a role in the lymphoid stromal organization within secondary lymphoid tissues. We report that adult CD4 ϩ CD3 Ϫ cells express high levels of mRNA for LT␣, LT␤, tumor necrosis factor (TNF) ␣, and LIGHT, which are the ligands for TNFR1 and the LT␤R. Levels of expression are comparable with those expressed in embryonic and neonatal CD4 ϩ CD3 Ϫ cells, and the expression of LT␤ is at least an order of magnitude greater than in CD11c ϩ DCs or plasmacytoid DCs (pDCs). Furthermore, using adoptive cell-transfer experiments, we demonstrate that the expression of these genes is functional: fetal CD4 ϩ CD3 Ϫ cells derived from embryonic day (E) 15 spleen and adult CD4 ϩ CD3 Ϫ cells, but not lymphocytes, pDCs, and DCs, are able to restore a significant degree of B/T segregation in the spleens of LT␣ Ϫ/Ϫ mice, and up-regulate VCAM-1 and CCL21 protein expression on the stroma.Using confocal microscopy, we demonstrate that this CD4 ϩ CD3 Ϫ cell associates closely with VCAM-1 ϩ follicular dendritic cells (FDCs) in B-cell areas as well as with the VCAM-1 ϩ stromal population within the T zone. Materials and ...

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Blood vessels in human immunodeficiency virus‐related lymphadenopathy: high endothelial venules and lymphocyte migration

Cited by 2 publications

References 13 publications

Innate control of adaptive immunity via remodeling of lymph node feed arteriole

Innate control of adaptive immunity via remodeling of lymph node feed arteriole

Function of CD4+CD3− cells in relation to B- and T-zone stroma in spleen

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