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Immune Reconstitution after Hematopoietic Stem Cell Transplantation
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Andreas Thiel, Tobias Alexander, Christian A. Schmidt, Falk Hiepe, Renate Arnold, Andreas Radbruch, Larissa Verda, Richard K. Burt
SHM, gene conversion, and CSR take place in germinal center B cells in response to BCR antigen stimulation. This results in high affinity antibodies with specialized effector functions. The reactions are dependent on T cell and germinal center follicular (epithelial) cell help.71 T cells communicate with B cells via a number of membrane bound receptor ligand complexes such as B cell CD40 and T cell CD40 ligand (CD40L). Interaction of CD40 with CD40L promotes B cell proliferation and CSR.76 If the CD40-CD40L interaction is blocked, B cells cannot proliferate and produce immunoglobulin.77 Interestingly, most lymphomas are B cells arising in the lymph node germinal center and involve oncogene translocations possibly due to errors in targeting of the SHM and CSR enzymes.78
Potential Targets for Imaging Atherosclerosis
Published in Robert J. Gropler, David K. Glover, Albert J. Sinusas, Heinrich Taegtmeyer, Cardiovascular Molecular Imaging, 2007
David N. Smith, Mehran M. Sadeghi, Jeffrey R. Bender
A growing body of evidence illustrates monocyte-lymphocyte crosstalk in disease progression, which may be pertinent to the maintenance of chronic inflammation in atherosclerosis. CD 137, a receptor on monocytes, engages its ligand, 4-1BB, on circulating monocytes and T cells. The interaction of these proteins accounts for a monocyte proliferation above that expected by either G- or M-CSF alone (64,65). Antigen presenting cell (including monocyte)-lymphocyte interactions via CD80 (B7-1) and/or CD86 (B7-2)-CD28 engagement may also play a role. Murine knockouts of the genes encoding either B7-1 or -2 have smaller atherosclerotic lesions than wild-type mice, when crossed with cholesterol-fed, LDL-R-deficient mice (66). In this model, there is also a reduction in interferon-gamma production from murine T cells exposed to HSP60. CD40, a member of the TNF receptor family, is expressed on most leukocytes, and is critical for NKT and T cell activation. In turn, interferon-gamma from activated NKT and T cells induces the membrane expression of CD 40 via STAT-1a- mediated transcription (67). Furthermore, CD40L-CD40 interactions may stimulate adhesion molecule expression, even in the absence of cytokine stimulation (68).
The expression of microRNAs and exposure to environmental contaminants related to human health: a review
Published in International Journal of Environmental Health Research, 2022
Maria Rosaria Tumolo, Alessandra Panico, Antonella De Donno, Pierpaolo Mincarone, Carlo Giacomo Leo, Roberto Guarino, Francesco Bagordo, Francesca Serio, Adele Idolo, Tiziana Grassi, Saverio Sabina
Air pollution could alter intercellular communication by extracellular vesicles (EVs), such as MVs, that can transfer miRNAs between tissues (Pavanello et al. 2016). Rodosthenous et al. investigated relationship between short-, intermediate-, and long-term exposures to PM and levels of EV-miRNAs in a cohort of healthy adults. The profile of 800 miRNAs was screened using Nanostring Technologies’ nCounter® assay that revealed an association between long-term ambient PM exposure with increased levels of some EV – miRNAs circulating in serum; in silico analysis showed that their target genes (for example interleukin 6 – IL-6, C-X-C motif chemokine ligand 12 – CXCL12, vascular cell adhesion molecule 1 – VCAM-1, cluster of differentiation 40 – CD40, platelet-derived growth factor subunit beta – PDGFB, etc.) are linked to CVD-related pathways, such as inflammatory response, atherosclerosis, toll-like receptor (TLR) etc. (Rodosthenous et al. 2016).
Ozone exposure and pulmonary effects in panel and human clinical studies: Considerations for design and interpretation
Published in Journal of the Air & Waste Management Association, 2018
Frampton et al. (2017) exposed 87 older adults (ages 55–70 years) to either 0, 70, or 120 ppb ozone (randomized) for 3 hr in the MOSES (Multicenter Ozone Study in Older Subjects) study. During the exposures, participants exercised on a stationary bicycle, alternating 15 minutes of exercise with 15 minutes of rest. While the primary health outcomes were related to cardiovascular impacts, secondary outcomes included lung function decrements, airway inflammation as represented by sputum PMNs and soluble markers, and respiratory symptoms. Spirometry was conducted 30 min prior to exposure, immediately postexposure, and 1 day after exposure. Sputum was induced 1 day after exposure. Symptoms were evaluated 30 min prior to exposure, immediately postexposure, 3–4 hr postexposure, and 1 day after exposure. During clean air exposure, FEV1 and FVC increased compared with preexposure values, and this effect persisted the following day. These improvements in lung function were shown to be attenuated in a dose-dependent manner with ozone exposure. There were no changes in FEV1/FVC or FEF25-75, suggesting that bronchoconstriction was not occurring. A significant increase in the percent PMNs in sputum was noted 22 hr after exposure to 120 ppb ozone; no significant increase was observed after 70 ppb exposure. No significant changes in sputum cluster of differentiation 40 (CD40) ligand, interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), or total protein were observed. Ozone exposures did not significantly affect respiratory symptoms.