scholarly journals CD27 sustains survival of CTLs in virus-infected nonlymphoid tissue in mice by inducing autocrine IL-2 production

2010 ◽  
Vol 120 (1) ◽  
pp. 168-178 ◽  
Author(s):  
Victor Peperzak ◽  
Yanling Xiao ◽  
Elise A.M. Veraar ◽  
Jannie Borst
Keyword(s):  
Nonlymphoid Tissue

Preferential and persistent depletion of CCR5+T-helper lymphocytes with nonlymphoid homing potential despite early treatment of primary HIV infection

Blood ◽  
2001 ◽  
Vol 98 (10) ◽  
pp. 3169-3171 ◽  
Author(s):  
Roman Krzysiek ◽  
Annick Rudent ◽  
Laurence Bouchet-Delbos ◽  
Arnaud Foussat ◽  
Claudie Boutillon ◽  
...  
Keyword(s):  
Hiv Infection ◽  
Protective Immunity ◽  
Immune Functions ◽  
T Helper ◽  
Primary Hiv Infection ◽  
T Helper Lymphocytes ◽  
Immunodeficiency Virus ◽  
Nonlymphoid Tissue ◽  
Th Lymphocytes

Abstract Strains of human immunodeficiency virus (HIV) transmitted between individuals use the CCR5 coreceptor, but no preferential depletion of particular Th-lymphocyte subpopulations has been reported during primary HIV infection (PHI). In contrast, gut-associated Th lymphocytes are preferentially depleted in macaques recently infected by simian immunodeficiency virus. The expression of CCR5 and the intestinal homing receptor integrin α4β7 on subpopulations of Th lymphocytes was studied in 12 patients with PHI. There was a profound decrease of circulating α4β7+ Th lymphocytes and CCR5+ memory Th lymphocytes with nonlymphoid homing potential (CD62L−CD45RO+). Unlike other Th lymphocytes, this cell population remained depleted despite early control of viral replication under antiretroviral treatment. Therefore, HIV preferentially targets a specific CCR5+ subpopulation of Th lymphocytes early during infection, inducing its persistent depletion despite treatment. Protective immunity in vivo depends on Th lymphocytes carrying homing capacity to nonlymphoid tissue, and therefore these data may explain the persistent abnormalities of immune functions in patients infected with HIV.

scholarly journals CD44 is necessary for optimal contact allergic responses but is not required for normal leukocyte extravasation.

1993 ◽  
Vol 178 (2) ◽  
pp. 497-507 ◽  
Author(s):  
R L Camp ◽  
A Scheynius ◽  
C Johansson ◽  
E Puré
Keyword(s):  
Delayed Type Hypersensitivity ◽  
Adhesion Receptor ◽  
Inflammatory Site ◽  
Soluble Cd44 ◽  
Leukocyte Extravasation ◽  
Nonlymphoid Tissue ◽  
In Vivo Administration ◽  
Draining Lymph Nodes ◽  
Normal Leukocyte

The in vivo administration of certain monoclonal antibodies (mAbs) against the adhesion receptor, CD44, into normal mice induces both a modulation of CD44 from the surface of peripheral lymphocytes, and a concomitant increase in the amount of soluble CD44 in the serum. CD44-negative lymphocytes isolated from anti-CD44-treated mice exhibit normal homing patterns upon adoptive transfer, and are capable of reexpressing CD44 upon activation. The treatment of haptensensitized mice with anti-CD44 mAb inhibits their ability to mount a cutaneous delayed-type hypersensitivity (DTH) response within the first 24 h after hapten challenge. This inhibition reflects a block in both the edema and leukocyte infiltration of the cutaneous site of DTH, whereas the extravasation and accumulation of leukocytes in the draining lymph nodes progress normally. After 72 h, the leukocytes that extravasate into the site of antigen challenge express CD44. These results indicate that CD44 is not necessary for normal leukocyte circulation but is required for leukocyte extravasation into an inflammatory site involving nonlymphoid tissue.

scholarly journals An inflammatory checkpoint regulates recruitment of graft-versus-host reactive T cells to peripheral tissues

2006 ◽  
Vol 203 (8) ◽  
pp. 2021-2031 ◽  
Author(s):  
Ronjon Chakraverty ◽  
Daniel Côté ◽  
Jennifer Buchli ◽  
Pete Cotter ◽  
Richard Hsu ◽  
...  
Keyword(s):  
T Cells ◽  
Activated T Cells ◽  
Peripheral Tissues ◽  
Graft Versus Host ◽  
Two Photon ◽  
Graft Versus Leukemia ◽  
Donor T Cells ◽  
Nonlymphoid Tissue ◽  
Mixed Chimeras

Transfer of T cells to freshly irradiated allogeneic recipients leads to their rapid recruitment to nonlymphoid tissues, where they induce graft-versus-host disease (GVHD). In contrast, when donor T cells are transferred to established mixed chimeras (MCs), GVHD is not induced despite a robust graft-versus-host (GVH) reaction that eliminates normal and malignant host hematopoietic cells. We demonstrate here that donor GVH-reactive T cells transferred to MCs or freshly irradiated mice undergo similar expansion and activation, with similar up-regulation of homing molecules required for entry to nonlymphoid tissues. Using dynamic two-photon in vivo microscopy, we show that these activated T cells do not enter GVHD target tissues in established MCs, contrary to the dogma that activated T cells inevitably traffic to nonlymphoid tissues. Instead, we show that the presence of inflammation within a nonlymphoid tissue is a prerequisite for the trafficking of activated T cells to that site. Our studies help to explain the paradox whereby GVH-reactive T cells can mediate graft-versus-leukemia responses without inducing GVHD in established MCs.

Memory T cells in nonlymphoid tissue that provide enhanced local immunity during infection with herpes simplex virus

2009 ◽  
Vol 10 (5) ◽  
pp. 524-530 ◽  
Author(s):  
Thomas Gebhardt ◽  
Linda M Wakim ◽  
Liv Eidsmo ◽  
Patrick C Reading ◽  
William R Heath ◽  
...  
Keyword(s):  
T Cells ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Memory T Cells ◽  
Local Immunity ◽  
Simplex Virus ◽  
Nonlymphoid Tissue

scholarly journals GM-CSF Controls Nonlymphoid Tissue Dendritic Cell Homeostasis but Is Dispensable for the Differentiation of Inflammatory Dendritic Cells

Immunity ◽  
2012 ◽  
Vol 36 (6) ◽  
pp. 1031-1046 ◽  
Author(s):  
Melanie Greter ◽  
Julie Helft ◽  
Andrew Chow ◽  
Daigo Hashimoto ◽  
Arthur Mortha ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Dendritic Cell ◽  
Cell Homeostasis ◽  
Gm Csf ◽  
Inflammatory Dendritic Cells ◽  
Nonlymphoid Tissue

scholarly journals Prion strain-dependent tropism is maintained between spleen and granuloma and relies on lymphofollicular structures

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Iman Al-Dybiat ◽  
Mohammed Moudjou ◽  
Davy Martin ◽  
Fabienne Reine ◽  
Laetitia Herzog ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Lymphoid Tissue ◽  
Detection Method ◽  
Prion Diseases ◽  
Follicular Dendritic Cells ◽  
Prion Strain ◽  
Strain Type ◽  
Lymphoid Structures ◽  
Nonlymphoid Tissue ◽  
Strain Dependent

Abstract In peripherally acquired prion diseases, prions move through several tissues of the infected host, notably in the lymphoid tissue, long before the occurrence of neuroinvasion. Accumulation can even be restricted to the lymphoid tissue without neuroinvasion and clinical disease. Several experimental observations indicated that the presence of differentiated follicular dendritic cells (FDCs) in the lymphoid structures and the strain type are critical determinants of prion extraneural replication. In this context, the report that granulomatous structures apparently devoid of FDCs could support prion replication raised the question of the requirements for prion lymphotropism. The report also raised the possibility that nonlymphoid tissue-tropic prions could actually target these inflammatory structures. To investigate these issues, we examined the capacity of closely related prions, albeit with opposite lymphotropism (or FDC dependency), for establishment in experimentally-induced granuloma in ovine PrP transgenic mice. We found a positive correlation between the prion capacity to accumulate in the lymphoid tissue and granuloma, regardless of the prion detection method used. Surprisingly, we also revealed that the accumulation of prions in granulomas involved lymphoid-like structures associated with the granulomas and containing cells that stain positive for PrP, Mfge-8 but not CD45 that strongly suggest FDCs. These results suggest that the FDC requirement for prion replication in lymphoid/inflammatory tissues may be strain-dependent.

scholarly journals The origin and development of nonlymphoid tissue CD103+ DCs

2009 ◽  
Vol 206 (13) ◽  
pp. 3115-3130 ◽  
Author(s):  
Florent Ginhoux ◽  
Kang Liu ◽  
Julie Helft ◽  
Milena Bogunovic ◽  
Melanie Greter ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Lamina Propria ◽  
Regulatory Protein ◽  
Lymphoid Organ ◽  
The Other ◽  
Flt3 Ligand ◽  
Cd11b Expression ◽  
Cross Presentation ◽  
Nonlymphoid Tissue ◽  
Two Populations

CD103+ dendritic cells (DCs) in nonlymphoid tissues are specialized in the cross-presentation of cell-associated antigens. However, little is known about the mechanisms that regulate the development of these cells. We show that two populations of CD11c+MHCII+ cells separated on the basis of CD103 and CD11b expression coexist in most nonlymphoid tissues with the exception of the lamina propria. CD103+ DCs are related to lymphoid organ CD8+ DCs in that they are derived exclusively from pre-DCs under the control of fms-like tyrosine kinase 3 (Flt3) ligand, inhibitor of DNA protein 2 (Id2), and IFN regulatory protein 8 (IRF8). In contrast, lamina propria CD103+ DCs express CD11b and develop independently of Id2 and IRF8. The other population of CD11c+MHCII+ cells in tissues, which is CD103−CD11b+, is heterogenous and depends on both Flt3 and MCSF-R. Our results reveal that nonlymphoid tissue CD103+ DCs and lymphoid organ CD8+ DCs derive from the same precursor and follow a related differentiation program.

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