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I Enander

Publications and source records attributed to I Enander.

49 records · Page 3Linked to original sources

Origin of the autoreactive anti-type II collagen response. II. Specificities, antibody isotypes and usage of V gene families of anti-type II collagen B cells.

Autoantibodies play an important role in the pathogenesis of type II collagen-induced arthritis in mice. We have earlier reported a high frequency of cells producing anti-CII autoantibodies and a low frequency of cells producing multispecific antibodies, in regional lymph nodes 9 to 11 days after primary immunization with CII. It is shown here that anti-CII antibodies produced during primary immune response are IgG-antibodies mainly of IgG2a, IgG1 and IgG2b subclasses while IgM antibodies dominate primary responses elicited by OVA and denatured CII as analyzed with a large panel of hybridomas. Anti-CII antibodies generated during the primary response recognize at least five different epitopes on the CII molecule. The specificities of these antibodies for various epitopes result from combinational association of products encoded by genes derived from various VH and VK families and/or by the occurrence of somatic mutations. It is suggested that the primary anti-CII autoantibody response involves activation of memory B cells and is in this aspect different from the origin of "natural" autoantibodies.

Animals↗

Immunological suppression of delayed hypersensitivity responses in mouse lungs as reflected by numbers of mononuclear cells, mast cells and mucus-producing cells.

The suppression of delayed hypersensitivity (DH) in the lung as reflected by the appearance of mononuclear cells, mast cells and mucus-producing cells was studied in Balb/c mice. Immunosuppression was induced by intravenous and peroral administration of picrylsulfonic acid (PSA) in mice subsequently sensitized with picrylchloride (PiCl). The animals exhibited a decreased DH reactivity as assessed by ear thickness increase compared with mice sensitized but not exposed to PSA pretreatment. In mice exposed to PSA intravenously (suppressed) and sensitized with PiCl there was a decrease in the number of mononuclear cells in the lung after challenge, compared to mice sensitized and challenged only. Similarly, the mast cell and mucus-producing cell numbers were slightly lower in animals immunosuppressed intravenously with PSA compared with sensitized mice. Such a decrease in the numbers of mononuclear cells, mast cells and mucus-producing cells in the lung was not seen in animals treated with PSA perorally, although these animals exhibited suppressed DH reaction in the ears. The present results indicate that induction of mononuclear cells and to some extent mast cells and mucus-producing cells in the lung relates to the DH reaction and its regulation.

Animals↗

Regulation by T cells of delayed hypersensitivity reaction in mouse lung as reflected by mononuclear cells, mast cells and mucus-producing cells.

The appearance of mononuclear cells, mast cells and mucus-producing cells in the lung and their linkage to the development of delayed hypersensitivity (DH) reactions were studied. Adoptive transfer of immune lymph node cells, spleen cells and serum and in vivo treatment with monoclonal antibodies to L3T4-positive T cells in Balb/c mice were performed to investigate the cellular regulation of the number of mononuclear cells, mast cells and mucus-producing cells in the lung. Immune lymph node cells and, to a lesser extent, immune spleen cells from mice sensitized epicutaneously with picrylchloride transferred DH reactions to the recipients as assessed by ear thickness increase after challenge. Serum from sensitized mice was not able to transfer a DH reaction. Cyclophosphamide treatment of donor mice increased the DH reaction in the recipient mice. Adoptive transfer of immune lymph node cells and spleen cells gave a slight increase in the number of mononuclear cells in the lung of recipient mice compared with controls. This weak accumulation of mononuclear cells in the lungs of recipient mice, however, was not accompanied by a consistent increase in the number of mucus-producing cells and mast cells. The number of spleen cells expressing the L3T4 antigen decreased after in vivo treatment with the monoclonal GK1.5 (anti-L3T4) antibody as assessed by immunohistochemistry. This antibody treatment also resulted in an inhibition of the DH reaction and a decrease in the number of mononuclear cells and mucus-producing cells, but not in mast cells in the lung of sensitized and challenged mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Immune regulation of goblet cell development.

In rats, goblet cells were found in the bronchiole epithelium surrounding enlarged lymphoid noduli. The goblet cell number increased with age. Old rats had goblet cells in the columnar epithelium. Immunization with aerosolized antigen increased goblet cell hyperplasia in bronchioli with a luminal diameter of 0.5-1.0 mm. In mice, goblet cell differentiation in the respiratory epithelium was caused by local delayed-type hypersensitivity reactions. Manipulations of the delayed hypersensitivity reactions with immune suppression and depletion of helper T cells eliminated the increase in goblet cell number.

Animals↗

Regulation of the delayed hypersensitivity reaction in the lung reflected as mononuclear, mast cell and mucus cell appearance after T helper cell depletion and adoptive transfer.

Epicutaneous sensitization with picrylchloride (PiCl) induced a strongly delayed hypersensitivity (DH) reaction in mice. Local challenge in the airways of these mice resulted in increased numbers of mononuclear cells, mast cells and mucus cells. Depletion of T helper cells in vivo by treatment with monoclonal antibody (GK 1.5) inhibited the DH reaction. This treatment also resulted in a decrease in the number of mononuclear and mucus cells in the lung after intranasal challenge. The DH reaction was transferred to recipients with immune lymph node cells and spleen cells from mice sensitized epicutaneously with PiCl. The recipient mice also showed a slight increase in the number of mononuclear cells in the lung after intranasal challenge. These results indicate that T cells are not only involved in the DH reaction but also in the accompanying lung reaction.

Animals↗

Cyclophosphamide-mediated enhancement of delayed hypersensitivity reactions in the lung.

The appearance of mononuclear cells, mast cells and mucous cells in the airways was studied in Balb/c mice in relation to cell-mediated immunity reflected as delayed hypersensitivity (DH). The animals were pretreated with cyclophosphamide (Cy) to increase cell-mediated immunity and to decrease the influence of antibodies. Mice pretreated with Cy and epicutaneously sensitized with picrylchloride (PiCl) had stronger DH reactions as compared with sensitized mice not pretreated with Cy. The Cy treatment decreased the IgG antibody formation after sensitization. The Cy-pretreated, sensitized and challenged mice had increased numbers of mucus-producing cells and to some extent also mononuclear cells in their lungs compared with sensitized and challenged non-Cy-treated animals. However, the mucous cell numbers were also increased in Cy-treated, but nonsensitized mice in which most of the airway epithelium had differentiated into mucus-containing cells. The present results indicate that local cell-mediated immunity involves the appearance of mononuclear cells and mucus-producing cells in the lung. This inflammatory reaction is enhanced by Cy treatment, although mucous cell differentiation seems to be induced by exposure to Cy alone.

Animals↗

Regional and systemic immune responses to trinitrophenyl derivatives after intranasal and subcutaneous sensitization of mice.

The immune responses and accompanying inflammatory local reactions were analyzed in mice sensitized subcutaneously (SC) or intranasally. Administration of picrylsulfonic acid (PSA) by both routes for two 2- or 1-week periods with a 4-week interval resulted in delayed hypersensitivity responses. Serum antibodies of the IgG and IgE and some of the IgA isotype were found, particularly in SC-sensitized animals. The latter animals also had levels of IgG antibodies in their bronchial fluid. Lymph node cells from mice sensitized for 2-week periods demonstrated high spontaneous proliferation. After culture together with spleen cells, these cells exhibited considerable numbers of mast cells, particularly after stimulation with pokeweed and antigen. The lungs from mice sensitized intranasally revealed increased numbers of mononuclear cells around large vessels and mucous cells in the bronchiolar epithelium, although there were individual differences between the animals. The mast cell numbers in the lungs were only slightly increased compared with numbers in nonimmunized animals subjected to ether anesthesia. Animals injected SC with PSA exhibited increased numbers of mast cells in their lungs compared with control mice. Mice sensitized with trinitrophenylated human serum albumin demonstrated some differences in their immune reactivity compared with animals immunized with PSA. Thus, no obvious delayed hypersensitivity appeared, but the IgG antibody titers were higher, and the IgE antibody titers were lower. The cellular responses assessed histologically demonstrated higher mononuclear cell numbers and lower mast cell numbers compared with those observed in animals sensitized with PSA.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Intranasal↗

Mononuclear cells, mast cells and mucous cells as part of the delayed hypersensitivity response to aerosolized antigen in mice.

Mice (BALB/c) exposed to picryl chloride (PiCl) on their shaved abdomen and untreated animals were after 7 days exposed to daily aerosolized trinitrophenylated dog serum albumin (TNP-DSA). Mice exposed to PiCl tended to respond earlier and more strongly with both delayed hypersensitivity (DH) and IgG antibodies in serum and bronchial washings than did mice exposed to aerosol only. Picryl chloride sensitization resulted in spontaneously proliferating axillary lymph node cells, which could not be further stimulated with antigen or mitogen. Histological examination of lung tissue of aerosol-sensitized animals revealed an increase in mononuclear cells and mast cells around bronchioli and mucous cells, particularly in those animals exposed for prolonged periods and sensitized with PiCl prior to aerosol. Sensitization of mice with aerosolized TNP-DSA administrated in two 2- and 1-week periods with a 4-week interval responded with DH and IgG antibody in a dose dependent fashion irrespective of presensitization with PiCl. In bronchial washings IgG antibodies were found particularly after two 2-week periods of exposure. The cells taken from the axillary or brachial lymph nodes showed spontaneous proliferation. Culture of the cells to achieve mast cell maturation resulted in no or very low numbers of mast cells in the lymph nodes.

Aerosols↗

Contact sensitivity in guinea pigs to different penicillins.

The ability of penicillins of varying lipophilicity to induce and elicit cellular allergic responses were analysed in guinea pigs. Epicutaneous application of the penicillins benzylpenicillin (Bp), cloxacillin (Clox) and Bacampicillin (Bamp) did not cause any unspecific skin irritation. Intracutaneously injected, however, Bamp, Clox and to a lesser extent Bp caused irritation at concentrations of 1.25%. Solutions of 0.12% of penicillins were inactive in this respect. Cellular allergic responses were induced with Bp, Bamp and Clox after repeated epicutaneous application. The magnitude of responses was related to the lipophilic properties of the penicillins, Bamp being superior. In the guinea pig maximization (GPM) test of Magnusson and Kligman employing intradermal injections of the penicillins with Freund's complete adjuvant, similar sensitizing abilities of the three penicillins were observed. The cellular allergic responses were elicited with Bp, Bamp, Clox and in addition ampicillin and the 1'-ethoxycarbonyloxyethyl ester of Bp. An extensive cross-reactivity between the penicillins was seen in Bp- and Bamp-sensitized animals, whereas the Clox-sensitized animals showed a specificity limited to Clox. Bamp was shown to possess a superior activity to elicit reactions, possibly due to its lipophilic properties together with an irritating effect exerted by the NH2 group.

Ampicillin↗