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Biomedical subjects

T Kakiuchi

Publications and source records attributed to T Kakiuchi.

At least 109 records · Page 6Linked to original sources
PubMed1987

Accessory cell function in a Con A response: role of Ia and interleukin 1.

Accessory cell (A-cell) function in a Con A response was analyzed. Irradiated P388D1 cells efficiently induced a proliferative response to Con A of T cells purified from spleen cells, whereas paraformaldehyde-fixed P388D1 cells failed to serve as A cells. Although IL-1 containing culture supernatant (SN) of a macrophage hybridoma induced the Con A response of the T-cell preparations, the depletion of Ia+ cells by the treatment with anti-Ia antibody and complement abrogated the response in the presence of IL-1. Fixed P388D1 cells and the hybridoma SN synergized in the reconstitution of the response. A 15,000-Da fraction of the hybridoma SN or human recombinant IL-1 alpha was able to substitute the hybridoma SN for the response. The reconstitution of the response by IL-1 and fixed P388D1 cells was inhibited by the addition of monoclonal anti-Ia antibody. These results indicate that IL-1 or fixed P388D1 cell does not exert a sufficient signal by itself and both of them are required for the reconstitution of a Con A response of highly purified T cells, and that Ia on fixed P388D1 cells play an important role.

Animals↗
PubMed1987

B cells as antigen-presenting cells: antigen-specific IL-2 production by cloned T cells without expression of IL-2 receptors.

A murine T cell clone, 24-2C, responds specifically to human IgG (HGG) in the context of I-Ab. B cells purified from mouse spleen cells were examined for their function as antigen-presenting cells (APC) in the response of 24-2C cells to HGG. B cells functioned as APC for IL-2 production but not for proliferation, whereas spleen cells or spleen-adherent cells functioned as APC for both IL-2 production and proliferation. LPS-activated B cells also failed to induce the proliferative response. The addition of the culture supernatant of 24-2C cells stimulated with HGG presented by irradiated spleen cells to the culture of 24-2C cells, irradiated B cells, and HGG induced the proliferative response of 24-2C cells, whereas IL-1, IL-3, and/or interferon-gamma did not reconstitute the proliferation. The expression of IL-2 receptors (IL-2R) on 24-2C cells was examined using a monoclonal anti-mouse IL-2R antibody AMT 13 or 7D4. 24-2C cells cultured with spleen cells as APC expressed IL-2R. Those cultured alone or with B cells as APC did not express IL-2R. Enlargement of 24-2C cells in response to HGG was also examined, and the relative cell size of those cultured with B cells or spleen cells as APC was larger than that of those cultured alone. These results demonstrate that B cells as APC induce IL-2 production and cell size enlargement in the response of 24-2C cloned T cells to HGG, but not IL-2R expression nor proliferation.

Animals↗
PubMed1987

The effect of cardiopulmonary bypass on T cells and their subpopulations.

To investigate the effect of cardiopulmonary bypass (CPB) on T cells, lymphocyte subsets of peripheral blood and lymphoid organs were monitored during and after open-heart surgery (Group 1). As a control, lymphocyte subsets of peripheral blood were measured in patients undergoing thoracovascular operations without CPB (Group 2). In Group 1, analysis of each subset-to-total lymphocyte ratio revealed that observed lymphocytopenia in the early postoperative days was mainly the result of T cell reduction, and that the decrease of helper/inducer T cells contributed to this decrease. In contrast, no significant fluctuation of any lymphocyte subpopulation ratio was observed in Group 2. Analysis of lymphocyte subpopulation ratios in lymphoid organs showed that reciprocal changes of T cells and their subsets were observed in the bone marrow, thus indicating that the redistribution of T cells (especially of helper/inducer cells) seems to occur between peripheral blood and bone marrow in Group 1. Furthermore, there was no relationship between serum cortisol levels and the changes in lymphocyte subset ratios in Group 1 patients.

B-Lymphocytes↗
PubMed1987

B cells as accessory cells in a Con A response of a T cell clone.

Accessory cell (AC) function of B cells was examined in Con A response of a cloned T cell line, 22-9D, which is Thy 1+,L3T4+,Lyt2-,H-2KbDb+ and I-Ab-.22-9D cells produced IL 2 in the presence of Con A without participation of AC. For the initiation of a proliferative response to Con A, the addition of spleen cells or spleen adherent cells was required. B cells as AC were unable to induce the proliferative response. In the presence of culture supernatant of spleen cells stimulated with Con A (CAS), 22-9D cells showed proliferative response to Con A with B cell AC. The response was inhibited by a relevant monoclonal anti-I-A antibody. Although irradiated spleen cells as AC induced IL 2 receptor expression of 22-9D cells in the presence of Con A, B cells were shown to require the addition of unknown factor(s) in CAS, which was suggested to be different from IL 1, IL 2, IL 3, or IFN-gamma, for the induction of the receptor expression on 22-9D cells.

Animals↗
PubMed1986

The regulatory role of sialic acids in the response of class II reactive T cell hybridomas to allogeneic B cells.

Two different kinds of alloreactive T cell hybridomas were established in previous experiments. One is reactive and the other is nonreactive to allogeneic I-A region-associated membrane antigen (mIa) on B cells. In the present experiments the difference between these hybridomas were analyzed by using representative clones, B cell mIa-reactive clone CB-11.4, and nonreactive clone HTB-9.3. Unresponsiveness of HTB-9.3 clone to allogeneic B cells could not be due to the inability of B cells in interleukin 1 production or the density of mIa molecules on B cells. HTB-9.3 clone could respond to C57BL/6 mouse B cells treated with neuraminidase (Nase), and Nase-treated HTB-9.3 clone could respond to normal B cells from C57BL/6 mouse, indicating that sialic acid on both B cells and HTB-9.3 clone plays a regulatory role in the alloreactivity of the clone. In response to B cells from C57BL/6 mouse, T cells from C3H/He mouse spleen showed similar reactivity to HTB-9.3 clone; that is, T cells could respond to Nase-treated B cells, and Nase-treated T cells to B cells, and T cells primed with C57BL/6 spleen cells in vitro showed similar reactivity to CB-11.4 clone. These results suggest that HTB-9.3 clone represents virgin T cells and CB-11.4 clone-primed T cells at least in alloreactivity. Anti-L3T4a was shown to block alloreactivities of both T cell hybridomas and splenic T cells against B cells more efficiently than against splenic adherent cells. These results suggest that L3T4a on T cell plays more important role in allogeneic response to B cells than to splenic adherent cells.

Animals↗
PubMed1986

B cells as antigen-presenting cells: antibody production in vitro against a T-dependent antigen.

It was examined whether B cells can serve as antigen-presenting cells (APC) in the antibody response to a T-dependent antigen, trinitrophenyl-ovalbumin (TNP-OVA). B cells purified from mice primed with TNP (TNP-B cells) responded to TNP-OVA in the presence of purified T cells sensitized with OVA (OVA-T cells). OVA-T cells required the addition of APC to proliferate in response to TNP-OVA. APC activity of TNP-B cells in the T-cell proliferation was abolished by 4000 R irradiation. Our experiments also revealed that an antibody response requires more adherent cells than the T-cell proliferation. These results indicate that adherent cells possibly accompanying the T- and B-cell preparations were at a less than functional level. There was genetic restriction between T and B cells for the antibody response. B cells in the pellet fraction of 70% Percoll density sedimentation behaved similarly to the unfractionated TNP-B cells in the antibody response. A T-cell clone specific for human gamma-globulin (HGG) also induced an anti-TNP antibody response in B cells from unprimed mice in the presence of TNP-HGG. These results suggest that B cells are able to elicit an antibody response to a T-dependent antigen in the presence of carrier-primed T cells without the participation of macrophages.

Animals↗
PubMed1986

Establishment of T-cell hybridoma constitutively producing macrophage-dependent T-cell replacing factor.

A T-cell hybridoma was established by the fusion of concanavalin A-stimulated splenic T cells with BW 5147. The hybridoma cells secrete a factor constitutively to support antibody formation of spleen cells depleted of T cells against TNP-Ficoll but not against horse red blood cells. The activity was indicated not to be due to interleukin 2, B-cell growth factor I, B-cell growth factor II, or interferon. The factor-mediated antibody response to TNP-Ficoll required the presence of adherent cells. The adherent cell function could be replaced by the macrophage culture supernatant containing interleukin 1. B cells responding to TNP-Ficoll in the culture with hybridoma factor were indicated to be Lyb 5+ and to bear receptors for third component of complement.

Animals↗
PubMed1986

Production of bone-resorbing activity and colony-stimulating activity in vivo and in vitro by a human squamous cell carcinoma associated with hypercalcemia and leukocytosis.

A squamous cell carcinoma of 33-yr-old patient who developed marked leukocytosis and hypercalcemia was transplanted into nude mice in which more marked leukocytosis and hypercalcemia also developed. This tumor (LJC-1-JCK) produced a colony-stimulating factor (CSF) and formed a cyst in the tumor from which a CSF-producing cell line (T3M-1) was established. The CSF causes predominantly formation of granulocytic colonies in addition to macrophage colonies. Bone-resorbing activity (BRA) was detected in the cystic fluid and was eluted as two separate peaks with proteins of an apparent molecular weight of 30,000-50,000 and 10,000-20,000. Colony-stimulating activity (CSA) was eluted at an apparent 30,000 mol wt. The conditioned medium of the T3M-1 cells also contained a BRA with an apparent 14,000 mol wt, whereas CSA eluted at an apparent 30,000 mol wt. PTH, epidermal growth factor, transforming growth factor-alpha, prostaglandin Es, and vitamin D could not account for the powerful BRA. In contrast to CSA, BRA was not inactivated by trypsin and more stable at 70 degrees C. When T3M-1 cells were transplanted into nude mice, marked hypercalcemia developed in addition to granulocytosis. Our findings suggest that the tumor produces and secretes a powerful BRA in vivo and in vitro, which is different from CSA in terms of molecular weight, heat stability, and trypsin treatment. We speculate that the synergistic action of CSF that stimulates macrophage colony formation and recruits osteoclast precursors, and BRA, which stimulates mononuclear phagocytes and/or osteoclasts were responsible for a marked increase in osteoclastic bone resorption and humoral hypercalcemia in the patient.

Animals↗
PubMed1985

Effect of priming with antigen on the expression of C3 receptors on murine B cells and the responses to TI-2 antigens.

The effect of priming with DNP-Ficoll on the expression of receptors for the third component of complement (CR) on B cells was studied. B cells from mice primed with antigen were separated into CR- and CR+ populations by rosetting and density gradient centrifugation, and they were examined for antibody responses to TI-2 antigens in vitro. CR- B cells in spleen cells from mice primed with antigen responded well in contrast with the low responsiveness of CR- B cells from unprimed mice. These CR- B cells from primed mice reached their peak responses 1 day earlier than CR+ B cells from primed or unprimed mice. The response of these CR- B cells was specific for the hapten used for priming, and the priming effect was most conspicuous in spleen cells from mice primed with antigen 3 days previously, and it decreased thereafter. The CR- B cells from primed mice also showed better responses than CR+ B cells to all polyclonal B cell activators (PBA) tested. When CR+ B cells were primed in vitro with DNP-Ficoll for 3 days, the major cell population responsive to the antigen in secondary culture was found to be CR- B cells. On the other hand, CR- B cells in spleens could not respond to DNP-Ficoll challenge after in vitro priming with the antigen for 3 days. These results indicate that B cells lose CR by priming with antigen, although they retain their responsiveness to antigens and PBA. The role of CR on B cells in the antibody response is discussed.

Animals↗
PubMed1985

Accessory cell function in the Con A response: role of Ia-positive and Ia-negative accessory cells.

We have examined the role of Ia-positive and Ia-negative accessory cells (AC) and soluble factors in Con A-stimulated murine T cell activation. Supernatant fluids containing interleukin 1 (IL 1) derived from the P388D1 macrophage cell line and from a lipopolysaccharide (LPS)-stimulated macrophage hybridoma provided only partial reconstitution of the response of purified T cells (18 to 27%). The complete reconstitution obtained with gamma-irradiated spleen cells or LPS-activated B cells was inhibited by approximately 60 to 77% when anti-Ia antibody was included in the culture. Despite this apparent involvement of Ia+ spleen AC, Ia-negative L cell AC could also reconstitute the response of both Class I-restricted Lyt-2+ T cells and Class II-restricted L3T4+ T cells. When the Ia-negative AC were employed, the L3T4 antigen on L3T4+ T cells played a critical role because addition of anti-L3T4 antibody to the culture inhibited the response by 85 to 90%. In contrast, anti-L3T4 did not inhibit the response in the presence of spleen AC. These results suggest that the molecules involved in T cell-AC interactions may vary depending on the AC source. Moreover, at least one of the putative target ligands for L3T4 presumably is not Ia, because anti-L3T4 inhibited T cell stimulation when Ia-negative AC were used.

Animals↗
PubMed1982

Different effect of LPS-induced macrophage factor on antibody responses to TI-1 and TI-2 antigens.

Effect of macrophage culture fluid (MF) on thymic independent (TI) antibody responses was examined. MF potentiated antibody responses of spleen cells to dinitrophenyl (DNP)-Ficoll and DNP-liposome, TI-2 antigens, but not to trinitrophenyl (TNP)-BA and TNP-LPS, TI-1 antigens. The enhancing effect of MF on the anti-DNP-Ficoll response was dose-dependent. Neither T cells nor macrophages were required for MF to exert the effect, suggesting that MF works on B cells directly. B cells modulated by MF in their antibody responses were indicated to be in mature B-cell subset for the following reasons: (i) the cells were in (CBA/N x BALB/c) F1 female but not in F1 male mice; (ii) the cells bore the receptors for C3 on their surface. MF was indicated to exert the enhancing effect on the antibody response by modulating the proliferation and/or early events in differentiation of B cells and not by promoting antibody secretion. The active component of the MF was indicated to be Interleukin 1.

Animals↗