33 research outputs found
IRF4 and BATF are critical for CD8(+) T-cell function following infection with LCMV.
CD8(+) T-cell functions are critical for preventing chronic viral infections by eliminating infected cells. For healthy immune responses, beneficial destruction of infected cells must be balanced against immunopathology resulting from collateral damage to tissues. These processes are regulated by factors controlling CD8(+) T-cell function, which are still incompletely understood. Here, we show that the interferon regulatory factor 4 (IRF4) and its cooperating binding partner B-cell-activating transcription factor (BATF) are necessary for sustained CD8(+) T-cell effector function. Although Irf4(-/-) CD8(+) T cells were initially capable of proliferation, IRF4 deficiency resulted in limited CD8(+) T-cell responses after infection with the lymphocytic choriomeningitis virus. Consequently, Irf4(-/-) mice established chronic infections, but were protected from fatal immunopathology. Absence of BATF also resulted in reduced CD8(+) T-cell function, limited immunopathology, and promotion of viral persistence. These data identify the transcription factors IRF4 and BATF as major regulators of antiviral cytotoxic T-cell immunity
Production and Decay of D_1(2420)^0 and D_2^*(2460)^0
We have investigated and final states and
observed the two established charmed mesons, the with mass
MeV/c and width MeV/c and
the with mass MeV/c and width
MeV/c. Properties of these final states, including
their decay angular distributions and spin-parity assignments, have been
studied. We identify these two mesons as the doublet predicted
by HQET. We also obtain constraints on {\footnotesize } as a function of the cosine of the relative phase of the two
amplitudes in the decay.Comment: 15 pages in REVTEX format. hardcopies with figures can be obtained by
sending mail to: [email protected]
Measurement of the branching fraction for
We have studied the leptonic decay of the resonance into tau
pairs using the CLEO II detector. A clean sample of tau pair events is
identified via events containing two charged particles where exactly one of the
particles is an identified electron. We find . The result is consistent with
expectations from lepton universality.Comment: 9 pages, RevTeX, two Postscript figures available upon request, CLNS
94/1297, CLEO 94-20 (submitted to Physics Letters B
Measurement of the Decay Asymmetry Parameters in and
We have measured the weak decay asymmetry parameters (\aLC ) for two \LC\
decay modes. Our measurements are \aLC = -0.94^{+0.21+0.12}_{-0.06-0.06} for
the decay mode and \aLC = -0.45\pm 0.31 \pm
0.06 for the decay mode . By combining these
measurements with the previously measured decay rates, we have extracted the
parity-violating and parity-conserving amplitudes. These amplitudes are used to
test models of nonleptonic charmed baryon decay.Comment: 11 pages including the figures. Uses REVTEX and psfig macros. Figures
as uuencoded postscript. Also available as
http://w4.lns.cornell.edu/public/CLNS/1995/CLNS95-1319.p
A measurement of B(D+S → φl+ν) B(D+S → φπ+)
Using the CLEO II detector at CESR, we have measured the ratio of branching fractions B (D + S → φl + ν) B (D + S → φπ + ) = 0.54 ± 0.05 ± 0.04 . We use this measurement to obtain a model dependent estimate of B (D + S → φπ + )
ADAM17 stabilizes its interacting partner inactive Rhomboid 2 (iRhom2) but not inactive Rhomboid 1 (iRhom1).
The metalloprotease ADAM17 (a disintegrin and metalloprotease 17) is a key regulator of tumor necrosis factor ? (TNF?), interleukin 6 receptor (IL-6R), and epidermal growth factor receptor (EGFR) signaling. ADAM17 maturation and function depend on the seven-membrane?spanning inactive rhomboid-like proteins 1 and 2 (iRhom1/2 or Rhbdf1/2). Most studies to date have focused on overexpressed iRhom1 and -2, so only little is known about the properties of the endogenous proteins. Here, we show that endogenous iRhom1 and -2 can be cell surface?biotinylated on mouse embryonic fibroblasts (mEFs), revealing that endogenous iRhom1 and -2 proteins are present on the cell surface and that iRhom2 also is present on the surface of lipopolysaccharide-stimulated primary bone marrow?derived macrophages. Interestingly, very little, if any, iRhom2 was detectable in mEFs or bone marrow?derived macrophages lacking ADAM17, suggesting that iRhom2 is stabilized by ADAM17. By contrast, the levels of iRhom1 were slightly increased in the absence of ADAM17 in mEFs, indicating that its stability does not depend on ADAM17. These findings support a model in which iRhom2 and ADAM17 are obligate binding partners and indicate that iRhom2 stability requires the presence of ADAM17, whereas iRhom1 is stable in the absence of ADAM17
Inclusive [eta] production in [tau] decays
We have searched for inclusive [eta] production in [tau] decays using a data sample of 2553 events of e+e- -->[tau]+[tau]- in the one-three topology. The data were obtained using the High Resolution Spectrometer at [radical sign]s=29 GeV. A 90% confidence level upper limit on the process [tau]+/- -->[pi]+/-[eta]X of 2.1% is found. Using [tau] decays to five charged particles limits of 0.5% on [tau]+/- -->[pi]+/-[eta][eta]X and 0.3% on [tau]+/- -->[pi]+/-[pi]+[pi]-[eta]X are also obtained.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26535/3/0000074.pd