T-Cell-Mediated Immunity and the Role of TRAIL in Sepsis-Induced Immunosuppression

ABSTRACT The immune response to lymphocytic choriomeningitis virus in mice lacking macrophage inflammatory protein-1α (MIP-1α) was evaluated. Generation of virus-specific effector T cells is unimpaired in MIP-1α-deficient mice. Furthermore, MIP-1α is not required for T-cell-mediated virus control or virus-induced T-cell-dependent inflammation. Thus, MIP-1α is not mandatory for T-cell-mediated antiviral immunity.

Download Full-text

Monoclonal antibodies to LFA-1 and to CD4 inhibit the mixed leukocyte reaction after the antigen-dependent clustering of dendritic cells and T lymphocytes.

Journal of Experimental Medicine ◽

10.1084/jem.165.5.1403 ◽

1987 ◽

Vol 165 (5) ◽

pp. 1403-1417 ◽

Cited By ~ 94

Author(s):

K Inaba ◽

R M Steinman

Keyword(s):

T Cells ◽

Dendritic Cells ◽

T Cell ◽

Cell Mediated Immunity ◽

Lymphocyte Function ◽

Mixed Leukocyte Reaction ◽

Binding Assays ◽

Lymphocyte Blastogenesis ◽

And Function

T cell proliferation in response to many stimuli is known to occur in discrete clusters of dendritic cells (DC) and CD4+ helper lymphocytes. The role of lymphocyte function-associated antigen (LFA-1) and CD4 in the formation and function of these clusters has been evaluated in the mixed leukocyte reaction (MLR). By day 1 of the control MLR, most of the DC and responsive T cells are associated in discrete aggregates. Addition of anti-LFA-1 and CD4 reagents does not block DC-T aggregation but reduces the subsequent proliferative response by 80-90%. Anti-LFA-1 disassembles newly formed DC-T cell aggregates, whereas anti-CD4 inhibits blastogenesis without disrupting the cluster. Binding of DC to sensitized, antigen-specific CD4+ cells has been studied using lymphoblasts isolated at day 4 of the MLR. It has been shown previously that greater than 80% blasts rebind to DC in an antigen-specific fashion in rapid (10 min) binding assays. Antigen-dependent DC-T binding is blocked by anti-Ia but not by mAb to LFA-1 or CD4. However, the bound anti-CD4-coated lymphocytes are unable to release IL-2. Anti-LFA-1-coated T cells release IL-2 but are easily disaggregated after binding to DC. These findings lead to two conclusions. LFA-1 and CD4 are not involved in the initial steps whereby DC bind to T cells but exert an independent and subsequent role. LFA-1 acts to stabilize the DC-T cluster, while CD4 contributes to lymphocyte blastogenesis and IL-2 release. Because DC but not other presenting cells cluster unprimed lymphocytes, it seems likely that an antigen-independent mechanism distinct from LFA-1 and CD4 mediates aggregate formation at the onset of cell-mediated immunity.

Download Full-text

1061The Role of CD4 T Cell Mediated Immunity in Pandemic Influenza Protection

Open Forum Infectious Diseases ◽

10.1093/ofid/ofu052.769 ◽

2014 ◽

Vol 1 (suppl_1) ◽

pp. S311-S311

Author(s):

Jennifer Nayak ◽

Andrea Sant ◽

Shabnam Alam

Keyword(s):

T Cell ◽

Pandemic Influenza ◽

Cd4 T Cell ◽

Cell Mediated Immunity

Download Full-text

R-Ras is required for murine dendritic cell maturation and CD4+ T-cell priming

Blood ◽

10.1182/blood-2011-05-357319 ◽

2012 ◽

Vol 119 (7) ◽

pp. 1693-1701 ◽

Cited By ~ 16

Author(s):

Gobind Singh ◽

Daigo Hashimoto ◽

Xiaocai Yan ◽

Julie Helft ◽

Patricia J.-Y. Park ◽

...

Keyword(s):

T Cell ◽

Mhc Class Ii ◽

Dendritic Cell Maturation ◽

Cell Mediated Immunity ◽

G Protein Signaling ◽

Protein Signaling ◽

Cell Responses ◽

Small G Protein ◽

Physiologic Function

Abstract R-Ras is a member of the RAS superfamily of small GTP-binding proteins. The physiologic function of R-Ras has not been fully elucidated. We found that R-Ras is expressed by lymphoid and nonlymphoid tissues and drastically up-regulated when bone marrow progenitors are induced to differentiate into dendritic cells (DCs). To address the role of R-Ras in DC functions, we generated a R-Ras-deficient mouse strain. We found that tumors induced in Rras−/− mice formed with shorter latency and attained greater tumor volumes. This finding has prompted the investigation of a role for R-Ras in the immune system. Indeed, Rras−/− mice were impaired in their ability to prime allogeneic and antigen-specific T-cell responses. Rras−/− DCs expressed lower levels of surface MHC class II and CD86 in response to lipopolysaccharide compared with wild-type DCs. This was correlated with a reduced phosphorylation of p38 and Akt. Consistently, R-Ras–GTP level was increased within 10 minutes of lipopolysaccharide stimulation. Furthermore, Rras−/− DCs have attenuated capacity to spread on fibronectin and form stable immunologic synapses with T cells. Altogether, these findings provide the first demonstration of a role for R-Ras in cell-mediated immunity and further expand on the complexity of small G-protein signaling in DCs.

Download Full-text

The Role of Macrophage Inflammatory Protein-1α/CCL3 in Regulation of T Cell-Mediated Immunity toCryptococcus neoformansInfection

The Journal of Immunology ◽

10.4049/jimmunol.165.11.6429 ◽

2000 ◽

Vol 165 (11) ◽

pp. 6429-6436 ◽

Cited By ~ 65

Author(s):

Michal A. Olszewski ◽

Gary B. Huffnagle ◽

Roderick A. McDonald ◽

Dennis M. Lindell ◽

Bethany B. Moore ◽

...

Keyword(s):

T Cell ◽

Cell Mediated Immunity ◽

Inflammatory Protein ◽

Macrophage Inflammatory Protein

Download Full-text

The Role of LIGHT in T Cell-Mediated Immunity

Immunologic Research ◽

10.1385/ir:30:2:201 ◽

2004 ◽

Vol 30 (2) ◽

pp. 201-214 ◽

Cited By ~ 23

Author(s):

Jing Wang ◽

Yang-Xin Fu

Keyword(s):

T Cell ◽

Cell Mediated Immunity ◽

Role Of Light

Download Full-text

Transfer of Mycoplasma hyopneumoniae-specific cell mediated immunity to neonatal piglets

Veterinary Research ◽

10.1186/s13567-021-00968-0 ◽

2021 ◽

Vol 52 (1) ◽

Author(s):

Evelien Biebaut ◽

Lisa Beuckelaere ◽

Filip Boyen ◽

Freddy Haesebrouck ◽

Charles-Oliver Gomez-Duran ◽

...

Keyword(s):

T Cells ◽

T Cell ◽

Mycoplasma Hyopneumoniae ◽

T Cell Subsets ◽

Cell Mediated Immunity ◽

Specific Cell ◽

Neonatal Piglets ◽

Tnf Α ◽

Primary Agent

AbstractMycoplasma hyopneumoniae is the primary agent of enzootic pneumonia in pigs. Although cell mediated immunity (CMI) may play a role in protection against M. hyopneumoniae, its transfer from sows to their offspring is poorly characterized. Therefore, maternally-derived CMI was studied in piglets from vaccinated and non-vaccinated sows. The potential influence of cross-fostering before colostrum ingestion on the transfer of CMI from dam to piglets was also investigated. Six M. hyopneumoniae vaccinated sows from an endemically infected herd and 47 of their piglets, of which 24 piglets were cross-fostered, were included, as well as three non-vaccinated control sows from an M. hyopneumoniae-free herd and 24 of their piglets. Vaccinated sows received a commercial bacterin intramuscularly at 6 and 3 weeks prior to farrowing. The TNF-α, IFN-γ and IL-17A production by different T-cell subsets in blood of sows, colostrum and blood of piglets was assessed using a recall assay. In blood of sows cytokine producing T-cells were increased upon M. hyopneumoniae vaccination. Similarly, M. hyopneumoniae-specific T-cells were detected in blood of 2-day-old piglets born from these vaccinated sows. In contrast, no M. hyopneumoniae-specific cytokine producing T-cells were found in blood of piglets from control sows. No difference was found in M. hyopneumoniae-specific CMI between cross-fostered and non-cross-fostered piglets. In conclusion, different M. hyopneumoniae-specific T-cell subsets are transferred from the sow to the offspring. Further studies are required to investigate the role of these transferred cells on immune responses in piglets and their potential protective effect against M. hyopneumoniae infections.

Download Full-text