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J S Ellis

Publications and source records attributed to J S Ellis.

48 records · Page 3Linked to original sources
PubMed1992

Sensitization of allo-specific T lymphocytes in vivo: role of antigen-presenting cells.

The migratory behavior of antigen-presenting cells was investigated in vivo. Purified murine splenic dendritic cells and splenic and peritoneal macrophages were labelled and injected subcutaneously in the hind foot-pads of mice and monitored for seven days. In the first 24 h, a small quantity of label was recovered from popliteal but not inguinal lymph nodes with radioactive (111In-oxine and 3H-uridine) but not fluorescent (1,1'-dioctadecyl 3,3,3'3'-tetramethylindocarbocyanine perchlorate and fluorescein isothiocyanate) labelling of the antigen-presenting cells. Chemical fixation of the injected antigen-presenting cells had no effect on the detection of label in the popliteal lymph nodes, suggesting that it was unlikely to be due to active cellular migration. Label recovery from hind feet declined with time over the seven day period and was independent of the label type. Essentially the same observations were made whether the antigen-presenting cells were syngeneic or allogeneic to the injected mice and irrespective of the type of antigen-presenting cell used. However, allogeneic antigen-presenting cells, which did not migrate to the draining lymph nodes, successfully primed T lymphocytes in these lymph nodes as shown by a secondary in vitro mixed leukocyte reaction. Again, chemical fixation of the injected antigen-presenting cells had no effect on their ability to prime allogeneic T lymphocytes in the draining lymph nodes. These experiments suggest that, during experimental allo-sensitization via the subcutaneous route, indirect priming of allogeneic T lymphocytes may be a dominant pathway.

Animals↗
PubMed1992

Adjuvant composition determines the induction of type II collagen-induced arthritis.

In this study we have investigated the influence of adjuvant composition on the development of collagen-induced arthritis and of anti-collagen type II specific B- and T-cell responses following immunization with type II collagen. DBA/l mice immunized with bovine collagen type II emulsified in complete Freund's adjuvant (CFA) containing Mycobacterium tuberculosis strain H37Ra developed footpad swelling indicative of arthritis. Animals immunized with collagen type II plus CFA containing Mycobacterium butyricum, or incomplete Freund's adjuvant showed no significant increase in footpad width. Induction of anti-CII specific T-cell proliferation was also dependent upon immunization with CII plus CFA containing M. tb H37RA. In contrast, ovalbumin-reactive T-cell proliferation was unaffected by the species of mycobacteria, indicating that the difference in adjuvant activity of the mycobacterial species is specific for anti-collagen type II T-cell responses. Antibody response to collagen type II, unlike T-cell responses, was not significantly different using the two adjuvants. This study therefore demonstrates that murine collagen-induced arthritis requires immunization with collagen type II together with complete Freund's adjuvant containing Mycobacterium tuberculosis H37RA. Since only this combination of antigen and adjuvant induces detectable arthritis and T-cell responses against collagen type II, while antibody synthesis does not have such stringent adjuvant requirements, this suggests that the development of the full pattern of the collagen-induced arthritis disease requires synergistic activation of both humoral and cell-mediated responses.

Adjuvants, Immunologic↗
PubMed1991

Chemically modified antigen-presenting cells induce T lymphocyte allospecific hyporesponsiveness.

We have investigated the interaction between murine T lymphocytes and allogeneic APC in an in vitro proliferative mixed leukocyte reaction. Our results demonstrate that freshly isolated potentially alloreactive murine splenic T lymphocytes, in primary culture, can be induced to develop a state of allospecific proliferative hyporesponsiveness in vitro by exposure to 1-ethyl-3-(3-dimethylaminopropyl)-carbodiimide-modified allogeneic APC, a method similar to that previously used to induce nonresponsiveness in murine Ag-specific self-MHC-restricted T lymphocyte clones. This hyporesponsiveness was: specific for the allohaplotype of inducing APC, maintained for 96 h in vitro, not due to cellular inhibitory mechanisms, and associated with reduced ability to secrete IL-2 but not IL-3. Induction of this hyporesponsiveness was not due to altered expression of class II MHC gene products on the APC but was associated with markedly reduced T lymphocyte-APC adhesive interactions despite the lack of a detectable immunophenotypic change in lymphocyte function-associated Ag 1 (LFA-1) and intercellular adhesion molecule 1 (ICAM-1) expression on the modified APC. Therefore, we propose that TCR occupancy in the absence of normal T lymphocyte-APC adhesive clustering may induce T lymphocyte tolerance.

Animals↗
PubMed1989

Diagnostic epidural opioid technique.

Diagnostic epidural blocks were performed on 27 chronic pain patients sequentially using saline, fentanyl, and lidocaine solution. The patients were divided into one of four groups based on their response to the epidural solutions: placebo response group--pain relief with placebo solutions; fentanyl response group--pain relief with epidural fentanyl; lidocaine response group (LRG)--pain relief with lidocaine but not fentanyl; and no response group--no pain relief with any of the solutions used. The four groups were compared on the basis of age, sex, site of pain, duration of pain, narcotic use, pain assessment index, and workmen's compensation claims. The comparisons resulted in the conclusion that LRG patients had a much longer average duration of pain than the other groups. On the basis of the information gathered, it was theorized that, despite their response to epidural lidocaine, LRG patients may actually be a group of operant pain patients. Their failure to receive analgesia from epidural fentanyl may be a learned response such that they associate any sensory input from the affected area as painful. If follow-up studies support these findings, then the diagnostic opioid technique may be a more sensitive tool in diagnosing chronic pain.

Adult↗
PubMed1986

Murine Gc globulin binds to a synthetic sequential polypeptide that is a murine B lymphocyte mitogen.

A non-immunoglobulin component in mouse serum was found to compete with antibody for the binding of a polyanionic antigen, poly (Tyr-Glu-Ala-Gly). The percent of the polymer (44 ng/ml) bound at physiological pH by the serum component in normal mouse serum was low (18%), but was much higher at pH 6.0 (85%). As a result, the binding of the polyanionic peptide antigen by antibody in immune serum was considerably lower at pH 6.0 than it was at physiological pH. These results should be taken into account when dealing with similar antigens that have been frequently studied in immunology, such as poly (Glu60 Ala40) and poly (Glu60 Ala30 Tyr10). The non-immunoglobulin serum component has been identified as Gc globulin, a vitamin D-binding protein that has been shown to be present on the surface of B lymphocytes. This binding might be responsible for the murine B cell mitogenicity of poly (Tyr-Glu-Ala-Gly) that has been previously reported.

Animals↗