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Biomedical subjects

C Webb

Publications and source records attributed to C Webb.

At least 145 records · Page 8Linked to original sources
PubMed1975

Inverse relationship between net electric charge on the antigen and that on the sensitized cell in cellular immune response: demonstration with basic encephalitogen of the brain.

An inverse relationship exists between the net-electrical charge of immunogens and the antibodies elicited (1). The cellular basis of the net charge phenomenon has been established for both positively and negatively charged immunogens, by cell separation techniques over columns of opposite charge (7, 8). To establish whether this phenomenon can be extended to include cell-mediated immunity, the response to basic encephalitogenic protein (BE) which induces experimental allergic encephalomyelitis (EAE) was now investigated. Lymph node cells from sensitized strain 13 guinea pigs were fractionated over positively and negatively charged columns and compared to unfractionated cell populations in two assay systems: (a) in vitro response to BE in terms of lymphocyte transformation and (b) the passive transfer of EAE to unsensitized syngeneic recipients. The response was found to be confined to the fraction of cells eluted from glass bead columns, namely, the more negative cells. Cells eluted from poly-L-lysine-coated glass bead columns (i.e., positive cells) were devoid of the capacity to respond to this antigen either in vivo or in vitro. It was previously established that thymocytes rather than bone marrow cells account for the inverse charge phenomenon as assayed by T-helper-cell function in in vivo antibody production (8). We have now extended the inverse charge effect to include cell-mediated immune response of the delayed hypersensitivity type.

Animals↗
PubMed1975

Immunological comparison of basic encephalitogen and histone F2A1.

The extent of immunological cross-reaction between basic encephalitogen and histone F2A1 on both the humoral antibody level and on the cellular level has been established. The extent of humoral cross-reaction was tested by direct complement fixation employing both anti-histone F2A1 and antisera to basic encephalitogen, by inhibition of complement fixation, by radioimmunoassay and by passive cutaneous anaphylaxis. The data obtained failed to reveal immunological cross-reaction at the cellular level was tested by the lymphocyte stimulation technique in rabbits and guinea pigs, by inhibition of lymphocyte stimulation and by delayed hypersensitivity skin reactions. A slight but significant cross-reaction between the two proteins on the cellular level was detected by inhibition of lymphocyte stimulation and by the delayed hypersensitivity test. It is concluded that the immunological studies provide limited evidence that the two proteins share antigenic determinants.

Animals↗
PubMed1975

Cellular immune response to peripheral nerve basic protein in idiopathic facial paralysis (Bell's palsy).

Lymphocytes from patients with Bell's palsy were shown to undergo significant stimulation when cultured in vitro in the presence of a purely neuritogenic basic protein (P1L) isolated from human peripheral nerve myelin. No sensitization was observed to other neural antigens, namely, another periperal nerve myelin basic protein (P2) and the central nerve myelin basic encephalitogenic protein (BE). A similar pattern of response was also demonstrated in patients with Guillain-Barré syndrome (GBS). Lymphocytes from patients suffering from other neuropathies or other diseases involving the face showed no response to any of these antigens. The specific in vitro response to P1L protein in Bell's palsy may suggest that an in vivo sensitization of lymphocytes to such self protein occurs in this condition, and that cell-mediated, probably post-infectious, autoimmune mechanisms may be an important factor in the pathogenesis of the paralysis. Thus, Bell's palsy is immunologically similar to GBS, or may even represent a mononeuritic variant of GBS. In view of these findings the administration of steroids to patients with Bell's palsy seems logical on the basis of their immunosuppressive action.

Adolescent↗
PubMed1975

Neuritogenic and encephalitogenic properties of the peripheral nerve basic proteins.

Two basic proteins, P1 of molecular weight 14,200 and P2 of molecular weight 12,300, purified from bovine peripheral nerve, were assayed for biological activity. The P1 protein is an exclusively neuritogenic agent, capable of producing clinical signs of experimental allergic neuritis (EAN) and histological abnormalities in the peripheral nervous system (PNS) of guinea pigs and rabbits, without any changes in their central nervous system (CNS). P2 protein, like the CNS basic encephalitogenic protein (BE), has combined neuritogenic and encephalitogenic activities, therefore it induces in these animals neurological signs and pathological evidence of EAN, as well as histological characteristics of experimental allergic encephalomyelitis (EAE).

Animals↗
PubMed1975

Cell-mediated immunity to neural antigens in idiopathic polyneuritis and myeloradiculitis. Clinical-immunologic classification of several autoimmune demyelinating disorders.

Patients with peripheral nervous system disorders were tested for the presence of cellular hypersensitivity to peripheral and central nervous system antigens by means of the in vitro lymphocyte transformation technique. Lymphocytes sensitized to the neuritogenic peripheral nervous system P1L basic protein were found in pure polyradiculitis of the Guillain-Barré syndrome type. Lymphocytes from patients with myeloradiculitis underwent transformation by peripheral P2 basic protein and by central nervous system basic encephalitogenic protein. In cases of chronic relapsing polyneuropathy response was shown to the central nervous system basic encephalitogen and to both of the peripheral nerve basic proteins. Lymphocytes from patients with other neurologic conditions showed no response to any oth these antigens. These findings suggest that cell mediated immunity to specific basic proteins of the myelin plays a rolw in the pathogenesis of the above-mentioned demyelinating disorders and may lead to a new approach in their classification and diagnosis.

Adult↗
PubMed1975

Cellular immune response to acetylcholine receptor-rich fraction, in patients with myasthenia gravis.

Lymphocytes from patients with myasthenia gravis were stimulated when cultured in vitro with an electric eel extract enriched in acetylcholine receptor. No stimulation was observed with other antigens from nerve or muscle origin. Lymphocytes from non-myasthenic patients showed no response to any of these antigens. These findings suggest that an in vivo sensitization of lymphocytes to self acetylcholine receptor may occur in myasthenia gravis. The presence of sensitized lymphocytes, probably resulting from an autoimmune mechanism, might be an important factor in the pathogenesis of the neuromuscular block in this disease.

Acetylcholine↗
PubMed1975

Fractionation of functional lymphocytes sensitized to basic encephalitogen on derivatized collagen and gelatin gels.

The lymph node cells of basic encephalitogen (BE)-sensitized guinea pigs were fractionated on derivatized collagen and gelatin gels. The population of cells specifically reactive to this antigen can be isolated from derivatized gelatin gels and retain their viability and functionality as assayed in vitro. The specific binding of BE-sensitized cells to BE-derivatized gels comprised between 1 and 2% of the cells applied per plate. The ratio of sensitized cells bound to non-sensitized cells bound ranged between 4 and 6. The viability and functionality of adherent cells detached from collagen gels after enzymatic degradation were impaired. In contrast, the responses obtained with the adherent cell population released from the gelatin gels, by melting at 37 degrees C, were equal or greater than those of the original unfractionated lymph node cell cultures. Furthermore, it was possible to obtain a nonadherent cell population which was virtually completely depleted of the capacity to respond to the sensitizing antigen.

Animals↗