<i>In vivo</i> maturation and migration of dendritic cells

Flores‐Romo, Leopoldo

doi:10.1046/j.1365-2567.2001.01204.x

Cited by 98 publications

(73 citation statements)

References 83 publications

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“…Central to pathways for activating tumor antigen-specific T cell and antibody responses is the uptake, processing, and presentation of the tumor antigen by dendritic cells (DC), professional antigen presenting cells [1,2]. The importance of endogenous DC has been highlighted by better clinical outcomes for patients with various tumor types when DC are found to be infiltrating the tumor [3,4].…”

Section: Introductionmentioning

confidence: 99%

The effect of anti-VEGF therapy on immature myeloid cell and dendritic cells in cancer patients

Osada

Chong

Tansik

et al. 2008

Cancer Immunol Immunother

274

177

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Impairment of dendritic cells (DC), the most effective activators of anti-cancer immune responses, is one mechanism for defective anti-tumor immunity, but the causes of DC impairment are incompletely understood. We evaluated the association of impaired DC differentiation with angiogenesis-associated molecules D-dimer, vascular endothelial growth factor (VEGF), urokinase plasminogen activator and plasminogen activator inhibitor (PAI-1) in peripheral blood from 41 patients with lung, breast, and colorectal carcinoma. Subsequently, we studied the effect of administration of the anti-VEGF antibody (bevacizumab) on DC maturation and function in vivo. Compared with healthy volunteers, cancer patients had a bias towards the immunoregulatory DC2, had deficits in DC maturation after overnight in vitro culture, and had a significant increase in immature myeloid cell progenitors of DC (0.50 +/− 0.31% vs. 0.32 +/− 0.16%, respectively, p=0.011). A positive correlation was found between the percentage of DC2 and PAI-1 (R=0.50) and between immature myeloid cells and VEGF (R=0.52). Bevacizumab administration to cancer patients was associated with a decrease in the accumulation of immature progenitor cells (0.39 +/− 0.30 % vs. 0.27 +/− 0.24 %, p=0.012) and induced a modest increase in the DC population in peripheral blood (0.47 +/− 0.23 % vs. 0.53 +/− 0.30 %). Moreover, anti-VEGF antibody treatment enhanced allo-stimulatory capacity of DC and T cell proliferation against recall antigens. These data suggest that DC differentiation is negatively associated with VEGF levels and may be one explanation for impaired anti-cancer immunity, especially in patients with advanced malignancies.

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Section: Introductionmentioning

confidence: 99%

The effect of anti-VEGF therapy on immature myeloid cell and dendritic cells in cancer patients

Osada

Chong

Tansik

et al. 2008

Cancer Immunol Immunother

274

177

View full text Add to dashboard Cite

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“…The latter interactions lead to transcriptional activation of genes encoding the co-stimulatory molecules (6). By the time the DCs migrate from the site of infection to the draining lymph nodes (DLN), they have matured, present antigenic peptides, and express costimulatory molecules (7,8). In the DLN, the mature DCs interact with naïve T cells through both TCR-peptide/ MHC and CD28-CD80/CD86 and activate T cells by providing two stimulating signals.…”

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confidence: 99%

B7-H1 (PD-L1) on T cells is required for T-cell-mediated conditioning of dendritic cell maturation

Talay

Shen

Chen

et al. 2009

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

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Studies have shown that T-cell-dendritic cell (DC) interaction is required for efficient DC maturation. However, the identities of the molecules that mediate the interaction in vivo are largely unknown. Here, we show that maturation of DCs as well as CD8 T-cell responses were impaired in B7-H1-deficient (B7-H1 ؊/؊ ) mice to influenza virus infection. Both defects were restored by transferring B7-H1-expressing naïve T cells into B7-H1 ؊/؊ mice. Similarly, transferring DCs from wild-type mice or from RAG1 ؊/؊ mice that had been injected with B7-H1-expressing naïve T cells also restored CD8 T-cell responses in B7-H1 ؊/؊ mice. These results demonstrate that B7-H1 on naïve T cells is required to condition immature DCs to undergo efficient maturation when they encounter microbial infection. In return, the mature DCs stimulate a robust T-cell reponse against the infecting pathogen.DC conditioning ͉ DC matuation ͉ T cell activation

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“…The immature stage is able to capture antigens by several mechanisms such as macropinocytosis, phagocytosis, and receptor-mediated uptake, especially through lectin receptors such as Langerin͞CD207 (11) and DEC-205͞CD205 (12). Typically, these immature cells are located in nonlymphoid organs such as skin, trachea, intestine, vagina, etc., sites that are normally in contact with environmental antigens (13,14). In contrast, the mature stage is characterized by a high capacity for T cell stimulation and differentiation, and these cells are often located in secondary lymphoid organs (spleen, lymph nodes, and Peyer's patches).…”

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confidence: 99%

“…In contrast, the mature stage is characterized by a high capacity for T cell stimulation and differentiation, and these cells are often located in secondary lymphoid organs (spleen, lymph nodes, and Peyer's patches). In their immature stage, DCs express many receptors for antigen uptake as well as environmental sensing, e.g., Toll-like receptors, whereas in the more mature state, DCs express high levels of activation (CD25) (15) and costimulatory (CD40 and CD86) molecules important for T cell responses (14).…”

mentioning

confidence: 99%