Rapid turnover of the recirculating lymphocyte pool in vivo

Young, Alan J.; Hay, John B.

doi:10.1093/intimm/7.10.1607

Cited by 50 publications

(27 citation statements)

References 29 publications

(50 reference statements)

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“…To help distinguish between these possibilities, AMs were labeled by the intravenous injection of the red fluorescent dye PKH26; this is a highly amphipathic dye that is known to be taken up by macrophage populations and stable for approximately 1 month (19). One important characteristic of PKH26 labeling is that fluorescence intensity is halved at each cell division (20,21).…”

Section: Resultsmentioning

confidence: 99%

The Prolonged Life-Span of Alveolar Macrophages

Murphy

Summer

Wilson

et al. 2008

Am J Respir Cell Mol Biol

171

124

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To further examine the half-life of alveolar macrophages, chimeric CD 45.2 mice were generated through bone marrow transplantation of donor CD 45.1 cells. Before administration of donor cells, recipient mice were divided into two cohorts: the first cohort received total body irradiation; the second cohort also received irradiationhowever, the thorax, head, and upper extremities were shielded with lead. Flow cytometric analysis was then performed on blood, peritoneal, and bronchoalveolar lavage cells over time to quantify engraftment. The data generated for the unshielded cohort of mice revealed a macrophage half-life of 30 days. In the shielded cohort, however, we found that by 8 months there was negligible replacement of recipient alveolar macrophages by donor cells, despite reconstitution of the blood and peritoneum by donor bone marrow. Consistent with these findings, the mean fluorescent intensity of alveolar macrophages remained stable over a 4-week period after in vivo PKH26 dye loading. Together, these data show that previous alveolar macrophage half-life studies were confounded by the fact that they did not account for the toxic effects of irradiation conditioning regimens, and demonstrate that the bone marrow does not significantly contribute to the alveolar macrophage compartment during steady-state conditions.

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Section: Resultsmentioning

confidence: 99%

The Prolonged Life-Span of Alveolar Macrophages

Murphy

Summer

Wilson

et al. 2008

Am J Respir Cell Mol Biol

171

124

View full text Add to dashboard Cite

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“…However, it does not explain the presence of infectivity in platelets and CD14 ϩ cells. Indeed, these two cellular subsets do not reach and/or recirculate from the lymphoid germinal centers (42). Considering the short life of platelets (3 days) (36) and short residence time of monocytes in blood (3 days) (41), an alternative hypothesis is that a certain cell lineage in bone marrow is the origin of infectivity in these cells.…”

Section: Discussionmentioning

confidence: 99%

Prionemia and Leukocyte-Platelet-Associated Infectivity in Sheep Transmissible Spongiform Encephalopathy Models

Lacroux

Vilette

Fernández‐Borges

et al. 2012

J Virol

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The dynamics of the circulation and distribution of transmissible spongiform encephalopathy (TSE) agents in the blood of infected individuals remain largely unknown. This clearly limits the understanding of the role of blood in TSE pathogenesis and the development of a reliable TSE blood detection assay. Using two distinct sheep scrapie models and blood transfusion, this work demonstrates the occurrence of a very early and persistent prionemia. This ability to transmit disease by blood transfusion was correlated with the presence of infectivity in white blood cells (WBC) and peripheral blood mononucleated cells (PBMC) as detected by bioassay in mice overexpressing the ovine prion protein PrP (tg338 mice) and with the identification of abnormal PrP in WBC after using protein misfolding cyclic amplification (PMCA). Platelets and a large variety of leukocyte subpopulations also were shown to be infectious. The use of endpoint titration in tg338 mice indicated that the infectivity in WBC (per ml of blood) was 10 6.5 -fold lower than that in 1 g of posterior brainstem sample. In both WBC and brainstem, infectivity displayed similar resistance to PK digestion. The data strongly support the concept that WBC are an accurate target for reliable TSE detection by PMCA. The presence of infectivity in short-life-span blood cellular elements raises the question of the origin of prionemia.

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“…In parallel, the serum of each sheep was analyzed for BLV seropositivity by immunodiffusion and enzyme-linked immunosorbent assay techniques (25). Cannulae were surgically established in intestinal or prescapular efferent lymphatics to allow chronic sampling of lymph as previously described (34). Briefly, sheep were fasted for 24 h preceding surgery and anesthetized by intravenous injection of pentobarbital sodium (Nembutal; Abbott) or fluothane (Covely) with closed-circuit anesthetic equipment.…”

Section: Methodsmentioning

confidence: 99%

Peripheral Blood B-Cell Death Compensates for Excessive Proliferation in Lymphoid Tissues and Maintains Homeostasis in Bovine Leukemia Virus-InfectedSheep

Debacq

Gillet

Asquith

et al. 2006

J Virol

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The size of a lymphocyte population is primarily determined by a dynamic equilibrium between cell proliferation and death. Hence, lymphocyte recirculation between the peripheral blood and lymphoid tissues is a key determinant in the maintenance of cell homeostasis. Insights into these mechanisms can be gathered from large-animal models, where lymphatic cannulation from individual lymph nodes is possible. In this study, we assessed in vivo lymphocyte trafficking in bovine leukemia virus (BLV)-infected sheep. With a carboxyfluorescein diacetate succinimidyl ester labeling technique, we demonstrate that the dynamics of lymphocyte recirculation is unaltered but that accelerated proliferation in the lymphoid tissues is compensated for by increased death in the peripheral blood cell population. Lymphocyte homeostasis is thus maintained by biphasic kinetics in two distinct tissues, emphasizing a very dynamic process during BLV infection.In vertebrates, continuous recirculation of lymphocytes from blood through tissues and lymph nodes is critical for protection of the host during pathological inflammatory processes, as well as physiological emigration of lymphocytes that participate in immune surveillance (1,4,6,11,16,33). The network of exchange between blood and lymph through the lymph node is absolutely required to maintain normal cell homeostasis. The presence of homeostatic control of lymphocyte numbers ensures an equilibrium where cell production equals cell loss. In an immune system where lymphocyte production is continuous and the total number of cells is constant, each newly produced lymphocyte can only survive if another one dies; i.e., the rate of peripheral cell renewal depends on the life span of peripheral cells. However, the life expectancy of a lymphocyte is not an intrinsic property of the cell but is determined by factors such as the environment, viral infections, and the presence or absence of another, competing, cell population. We previously studied lymphocyte homeostasis, more particularly, lymphocyte proliferation and death, in different animal models of chronic leukemia, including sheep infected by the bovine leukemia virus (BLV) (7-9). In this model, proliferation was estimated by intravenous injection of bromodeoxyuridine (BrdU), a thymidine analog which is incorporated into the newly synthesized DNA via the pyrimidine salvage pathway. Although BrdU uptake by cells might occur in blood, its incorporation is thought to occur mainly, if not exclusively, in lymphoid tissues such as the lymph nodes, the spleen, or the bone marrow (7). By this approach, the estimated B-cell proliferation rates in infected and control sheep were 0.020 day Ϫ1 and 0.011 day Ϫ1 , respectively, meaning that 2.0 and 1.1% of the cells were produced by proliferation in 1 day. In contrast, the death rates of BrdU-labeled cells were not significantly different between the two categories of animals (average death rate, 0.089 day Ϫ1 versus 0.094 day Ϫ1 , respectively). The imbalance created by the net increase in proliferation ...

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Rapid turnover of the recirculating lymphocyte pool in vivo

Cited by 50 publications

References 29 publications

The Prolonged Life-Span of Alveolar Macrophages

The Prolonged Life-Span of Alveolar Macrophages

Prionemia and Leukocyte-Platelet-Associated Infectivity in Sheep Transmissible Spongiform Encephalopathy Models

Peripheral Blood B-Cell Death Compensates for Excessive Proliferation in Lymphoid Tissues and Maintains Homeostasis in Bovine Leukemia Virus-InfectedSheep

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