18 research outputs found
ΠΠΎΠ΄Π΅Π»ΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ ΡΠΎΡΠΌΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΡΡΡΡΠΊΡΡΡΡ ΠΌΠ΅ΡΠ°Π»Π»ΠΎΠΌΠ°ΡΡΠΈΡΠ½ΡΡ ΠΊΠΎΠΌΠΏΠΎΠ·ΠΈΡΠΎΠ² Π² ΠΏΡΠΎΡΠ΅ΡΡΠ΅ ΡΠΈΠ½ΡΠ΅Π·Π° Ρ ΠΎΡΠ΅Π½ΠΊΠΎΠΉ ΡΡΡΠ΅ΠΊΡΠΈΠ²Π½ΡΡ ΡΠ²ΠΎΠΉΡΡΠ²
Π Π°Π±ΠΎΡΠ° ΠΏΠΎΡΠ²ΡΡΠ΅Π½Π° ΠΌΠΎΠ΄Π΅Π»ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΏΡΠΎΡΠ΅ΡΡΠ° ΠΊΡΠΈΡΡΠ°Π»Π»ΠΈΠ·Π°ΡΠΈΠΈ ΠΊΠΎΠΌΠΏΠΎΠ·ΠΈΡΠ° Ρ ΠΌΠ΅ΡΠ°Π»Π»ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΌΠ°ΡΡΠΈΡΠ΅ΠΉ ΠΈ ΡΠ²Π΅ΡΠ΄ΡΠΌΠΈ Π²ΠΊΠ»ΡΡΠ΅Π½ΠΈΡΠΌΠΈ Ρ ΡΡΠ΅ΡΠΎΠΌ ΡΡΠ»ΠΎΠ²ΠΈΠΉ ΡΠΈΠ½ΡΠ΅Π·Π° (Π΄Π°Π²Π»Π΅Π½ΠΈΠ΅, ΡΠΊΠΎΡΠΎΡΡΡ ΠΎΡ
Π»Π°ΠΆΠ΄Π΅Π½ΠΈΡ), ΠΌΠΎΠ΄Π΅Π»ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΏΡΠΎΡΠ΅ΡΡΠ° ΡΠΎΡΠΌΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΏΠ΅ΡΠ΅Ρ
ΠΎΠ΄Π½ΠΎΠΉ Π·ΠΎΠ½Ρ ΠΌΠ΅ΠΆΠ΄Ρ ΡΠ°ΡΡΠΈΡΠ°ΠΌΠΈ ΠΈ ΠΌΠ°ΡΡΠΈΡΠ΅ΠΉ ΠΈ ΡΠ°ΡΡΠ΅ΡΡ ΡΡΡΠ΅ΠΊΡΠΈΠ²Π½ΡΡ
ΡΠ²ΠΎΠΉΡΡΠ² ΠΏΠΎΠ»ΡΡΠ°Π΅ΠΌΡΡ
ΠΊΠΎΠΌΠΏΠΎΠ·ΠΈΡΠΎΠ².The work is devoted to modeling the crystallization process of metal matrix composite with solid inclusions, taking into account the synthesis conditions (pressure, cooling rate), to modeling the formation of the transition zone between particles and matrix, and calculating the effective properties of the resulting composites
Single-cell analysis by mass cytometry reveals metabolic states of early-activated CD8+ T cells during the primary immune response
Memory T cells are thought to rely on oxidative phosphorylation and short-lived effector T cells on glycolysis. Here, we investigated how T cells arrive at these states during an immune response. To understand the metabolic state of rare, early-activated T cells, we adapted mass cytometry to quantify metabolic regulators at single-cell resolution in parallel with cell signaling, proliferation, and effector function. We interrogated CD8+ T cell activation in vitro and in response to Listeria monocytogenes infection in vivo. This approach revealed a distinct metabolic state in early-activated T cells characterized by maximal expression of glycolytic and oxidative metabolic proteins. Cells in this transient state were most abundant 5 days post-infection before rapidly decreasing metabolic protein expression. Analogous findings were observed in chimeric antigen receptor (CAR) T cells interrogated longitudinally in advanced lymphoma patients. Our study demonstrates the utility of single-cell metabolic analysis by mass cytometry to identify metabolic adaptations of immune cell populations in vivo and provides a resource for investigations of metabolic regulation of immune responses across a variety of applications
Trichomonas vaginalis homolog of macrophage migration inhibitory factor induces prostate cell growth, invasiveness, and inflammatory responses
The human-infective parasite Trichomonas vaginalis causes the most prevalent nonviral sexually transmitted infection worldwide. Infections in men may result in colonization of the prostate and are correlated with increased risk of aggressive prostate cancer. We have found that T. vaginalis secretes a protein, T. vaginalis macrophage migration inhibitory factor (TvMIF), that is 47% similar to human macrophage migration inhibitory factor (HuMIF), a proinflammatory cytokine. Because HuMIF is reported to be elevated in prostate cancer and inflammation plays an important role in the initiation and progression of cancers, we have explored a role for TvMIF in prostate cancer. Here, we show that TvMIF has tautomerase activity, inhibits macrophage migration, and is proinflammatory. We also demonstrate that TvMIF binds the human CD74 MIF receptor with high affinity, comparable to that of HuMIF, which triggers activation of ERK, Akt, and Bcl-2βassociated death promoter phosphorylation at a physiologically relevant concentration (1 ng/mL, 80 pM). TvMIF increases the in vitro growth and invasion through Matrigel of benign and prostate cancer cells. Sera from patients infected with T. vaginalis are reactive to TvMIF, especially in males. The presence of anti-TvMIF antibodies indicates that TvMIF is released by the parasite and elicits host immune responses during infection. Together, these data indicate that chronic T. vaginalis infections may result in TvMIF-driven inflammation and cell proliferation, thus triggering pathways that contribute to the promotion and progression of prostate cancer