Immunological memory transferred with CD4 T cells specific for tuberculosis antigens Ag85B-TB10.4: persisting antigen enhances protection.

Background: High levels of death and morbidity worldwide caused by tuberculosis has stimulated efforts to develop a new vaccine to replace BCG. A number of Mycobacterium tuberculosis (Mtb)-specific antigens have been synthesised as recombinant subunit vaccines for clinical evaluation. Recently a fusion protein of TB antigen Ag85B combined with a second immunodominant TB antigen TB10.

Cyclical expression of L-selectin (CD62L) by recirculating T cells.

L-Selectin (CD62L) mediates T-cell entry into lymph nodes. Whether the microenvironment modulates L-selectin expression of T cells during diapedesis and transit is unknown. Therefore, L-selectin expression was determined quantitatively on circulating T cells in blood, lymph nodes and thoracic duct by confocal laser scanning microscopy.

CD4 memory T cells on trial: immunological memory without a memory T cell.

Immunological memory crucially depends on CD4 T cells. In contrast with B cells, we find no decisive evidence that CD4 T cells are permanently altered by antigen stimulation. We propose that the memory response is derived from an increase in frequency of resting naïve-like CD4 T cells with a half-life of years (or months in rodents), rather than the currently proposed specialized T-cell types that have a known lifespan of days.

Transgenic CD4 T cells (DO11.10) are destroyed in MHC-compatible hosts by NK cells and CD8 T cells.

During an immune response a small number of rare Ag-specific clones proliferate extensively and decline, leaving a residual population for long-term memory. TCR transgenic (tg) CD4 T cells have been used widely to study the primary and memory response in vivo. We show here that naive TCR tg CD4 T cells from the DO11.

On the role of CD26 in CD4 memory T cells.

We studied an in vivo mouse model to evaluate the relationships between CD26--a glycoprotein with dipeptidyl peptidase IV (DPP-IV) activity implicated in the regulation of immune functions--and T cells expressing the effector/memory phenotype CD45RB. We report that CD26 does not define a differentiation stage of CD4 T cells because the density and frequency of CD26 on CD4 T cells from the spleen, inguinal and mesenteric lymph node was similar within the CD45RB+ (naïve) and CD45RB- (antigen primed) subsets. This observation was confirmed using CD4 T cells from a T-cell receptor transgenic (tg) model.

Naive T-cell receptor transgenic T cells help memory B cells produce antibody.

Injection of the same antigen following primary immunization induces a classic secondary response characterized by a large quantity of high-affinity antibody of an immunoglobulin G class produced more rapidly than in the initial response - the products of memory B cells are qualitatively distinct from that of the original naive B lymphocytes. Very little is known of the help provided by the CD4 T cells that stimulate memory B cells. Using antigen-specific T-cell receptor transgenic CD4 T cells (DO11.

Mobilisation of specific T cells from lymph nodes in contact sensitivity requires substance P.

Capsaicin-mediated depletion of neuropeptides in the skin was previously shown to abolish a dinitrocholorobenzene (DNCB)-induced contact sensitivity (CS) response. To understand the basis for this disruption, we explored whether nerve fibres innervating the draining lymph node (LN) could be involved. As expected, removal of the draining LN after DNCB sensitisation abolished the CS response.

Naive, effector, and memory T lymphocytes efficiently scan dendritic cells in vivo: contact frequency in T cell zones of secondary lymphoid organs does not depend on LFA-1 expression and facilitates survival of effector T cells.

Contact between T cells and dendritic cells (DCs) is required for their subsequent interaction leading to the induction of adaptive immune responses. Quantitative data regarding the contact frequencies of T cell subsets in different lymphoid organs and species are lacking. Therefore, naive, effector, and memory CD4 T cells were injected into rats in absence of the cognate Ag, and 0.

Nerve fibres are required to evoke a contact sensitivity response in mice.

Previous work has indicated that the dermis and epidermis of skin contains abundant nerve fibres closely associated with Langerhans' cells. We have investigated whether these nerve endings are necessary for inducing and evoking a contact sensitivity (CS) response. Topical application of a general or a peptide (calcitonin gene-related peptide and substance P)-specific neurotoxin was employed to destroy the nerve fibres at skin sites subsequently used to induce or evoke the CS response.

Inhibition of chronic vascular rejection by donor-specific blood transfusion is associated with a reduction in transforming growth factor-beta1 expression.

Background: Concentric intimal thickening and the infiltration of inflammatory cells in cardiac allografts are the pathological hallmark characteristics of chronic vascular rejection (CVR), the leading cause of long-term graft failure. The precise mechanisms involved in the development and pathogenesis of CVR remain elusive. In the PVG-R23 to PVG-RT1u rat model of CVR, prior administration of a donor-specific transfusion (DST) was previously shown to prolong graft survival indefinitely and abolish the vascular lesions associated with CVR.