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Biomedical subjects

T Hamaoka

Publications and source records attributed to T Hamaoka.

At least 253 records · Page 14Linked to original sources
PubMed1986

The augmentation of tumor-specific immunity by virus help. III. Enhanced generation of tumor-specific Lyt-1+2- T cells is responsible for augmented tumor immunity in vivo.

The role of vaccinia virus-reactive helper T cells (Th) in augmenting in vivo generation of antitumor protective immunity and the Ly phenotype mediating the enhanced in vivo tumor immunity were investigated. C3H/HeN mice were inoculated i.p. with viable vaccinia virus to generate vaccinia virus-reactive Th activity. The mice were subsequently immunized i.p. with virus-infected syngeneic X5563 and MH134 tumor cells, and spleen cells from these mice were tested for in vivo tumor neutralizing activity. Immunization of virus-primed mice with virus-uninfected tumor cells and of virus-unprimed mice with virus-infected tumor cells failed to result in in vivo protective immunity. In contrast, spleen cells from mice immunized with virus-infected tumor cells subsequent to virus-priming exhibited potent tumor-specific neutralizing activities. Such an augmented generation of in vivo protective immunity was accompanied by enhanced induction of tumor-specific cytotoxic T lymphocyte (CTL) and antibody activities in X5563 and MH134 tumor systems, respectively. However, analysis of the effector cell type responsible for in vivo tumor neutralization revealed that enhanced in vivo immunity was mediated by Lyt-1+2- T cells in both tumor systems. Moreover, the Lyt-1+2- T cells exerted their function in vivo under conditions in which anti-X5563 tumor-specific CTL or anti-MH134 tumor-specific antibody activity was not detected in recipient mice. These results indicate that augmenting the generation of a tumor-specific Lyt-1+2- T cell population is essential for enhanced tumor-specific immunity in vivo.

Animals↗
PubMed1986

High plasma cholecystokinin response following ingestion of test meal by patients with non-insulin dependent diabetes mellitus.

Postprandial responses of plasma cholecystokinin (CCK) in patients with non-insulin dependent diabetes mellitus (NIDDM) were studied with a CCK specific radioimmunoassay. After the ingestion of a liquid test meal, plasma CCK levels increased from the basal level of 9.8 +/- 1.1 pg/ml to a peak of 19.4 +/- 1.8 pg/ml at 20 min in healthy subjects (n = 10). The ingestion of a test meal in patients with NIDDM (n = 10) resulted in a significantly greater increase of plasma CCK than in healthy subjects and a significant increase of plasma CCK from a basal level of 14.2 +/- 4.4 pg/ml to a peak of 47.4 +/- 12.4 pg/ml at 10 min.

Adult↗
PubMed1986

Effect of passive administration of alloantiserum containing antibody against putative acceptor(s) for T cell-replacing factor (TRF) in the neonatal stage on development of B cell activity responsive to TRF.

Previously, we showed that the antiserum raised in male (DBA/2Ha X BALB/c)F1(DCF1) mice (T cell-replacing factor [TRF]-low response animals) by immunizing them with activated B cells from BALB/c mice (TRF-high-responders) contained antibodies against putative TRF-acceptor site(s). We have now evaluated the hypothesis that neonatal treatment of mice with the above antiserum suppresses the development of B cells responsive to TRF. Male DCF1 mouse anti-BALB/c B-cell antiserum or normal DCF1 mouse serum as a control was injected into BALB/c mice within 24 hr after birth. In the antiserum-treated mice, no augmented primary immunoglobulin M (IgM) antibody responses to sheep red blood cells (SRBC) were observed under the conditions in which markedly augmented IgM anti-SRBC responses were induced in control BALB/c mice, suggesting that development of B cells reacting with male DCF1 mouse anti-BALB/c B-cell antiserum is suppressed by the neonatal treatment with the antiserum. Furthermore, the development of B cell activity responsible for helper factors derived from T cells, such as TRF, was markedly suppressed in the neonatally antiserum-treated mice, whereas activity of B cells capable of interacting directly with helper T cells through antigen-bridges was not significantly affected by the same treatment. Such suppression of the B cell activity could be induced only when the antiserum was administered within 48 hr after birth. Moreover, neonatal treatment of mice with the antiserum induced suppressed responsiveness of B cells to a T-independent type 2 antigen, TNP-Ficoll. Neither serum-borne suppressive serum components nor suppressor cells were detected by the system employed. These results support the hypothesis that TRF responsive B cells constitute a subpopulation distinct from the other B cells capable of cooperating with helper T cells via cognate interaction.

Animals↗
PubMed1986

Suppressive effect of ultraviolet-B-irradiation of epidermal cells on the induction of contact sensitivity.

Contact sensitivity to trinitrophenyl (TNP) hapten was induced by subcutaneous (s.c.) administration of TNP-modified syngeneic spleen cells or epidermal cells (EC) (TNP-EC). Intraperitoneal (i.p.) inoculation of TNP-EC resulted in a comparable response, whereas i.p. administration of TNP-spleen cells or TNP-modified-ultraviolet (UV)-preirradiated EC (TNP-UV-EC) failed to induce TNP-contact sensitivity responses. The present study investigates the effect of UV-irradiation on the potential of EC for inducing the contact sensitivity response. Exposure of BALB/c mouse EC in vitro to 1600 J/m2 of UV-B before they were modified with TNP had no discernible effect on the Ia-positivity and viability of EC. Coexistence of TNP-UV-EC had no inhibitory effect upon the contact sensitivity response induced by TNP-EC via the i.p. route. The absence of suppressor cell generation was substantiated by the adoptive transfer of spleen cells from mice administered TNP-UV-EC i.p. to normal syngeneic mice. The effect of interleukin 1 (IL-1) or epidermal cell-derived thymocyte-activating factor (ETAF) in restoring the ability of TNP-UV-EC to induce contact sensitivity was examined. IL-1 or ETAF administered along with TNP-spleen cells i.p. induced a potent contact sensitivity response, whereas the same preparations of IL-1 or ETAF were unable to restore the contact sensitivity induction by TNP-UV-EC. The results are discussed in the context of UV-induced cell surface changes of the Langerhans cell population.

Animals↗
PubMed1986

Role of L3T4 antigen in the activation of various functions of Lyt-1+2- T cells against vaccinia virus.

The present study defines assay systems for vaccinia virus-reactive Lyt-1+2- T cells mediating various functions and investigates the positivity of L3T4 antigen on these Lyt-1+2- T cells as well as the role of L3T4 antigen in the activation of these T cells with respect to their functions. C3H/He mice were immunized against vaccinia virus by inoculating viable virus intraperitoneally (i.p.). Anti-vaccinia virus reactivity in lymphoid cells from these immunized mice was assessed by proliferative response, helper T cell activities involved in cytotoxic T lymphocyte (CTL) and B cell (antibody) responses, delayed type-hypersensitivity (DTH) response, and production of lymphokines such as interleukin 2 (IL2) and macrophage-activating factor (MAF). The results demonstrate that all of the above anti-vaccinia virus responses were mediated by Lyt-1+2- T cells and that these Lyt-1+2- T cells expressed L3T4 antigens on their cell surfaces. Moreover, such anti-vaccinia Lyt-1+2- T cell responses were inhibited in the presence of anti-L3T4 antigen antibody. These results indicate that there is a reciprocal relationship between Lyt-2 and L3T4 markers, and that L3T4 antigen is closely related to the activation of various functions of anti-vaccinia virus Lyt-1+2- T cells.

Animals↗
PubMed1986

Cross-reactivity between haptenic muramyl di- or tripeptide derivatives and Mycobacterium bovis BCG: potential application for enhancing tumor immunity.

Muramyl di- or tripeptide (MDP or MTP) hapten derivatives bearing various structures were synthesized, and the correlation of these structures with cross-reactivity with Mycobacterium bovis BCG and their applicability to enhance induction of syngeneic tumor immunity were investigated. The cross-reactivity of MDP or MTP haptens to BCG was examined by T-cell proliferation responses of lymph node cells from BCG-primed C3H/He mice in the stimulation with MDP- or MTP-coupled syngeneic cells. A haptenic MDP derivative (designated L4-MDP) stimulated proliferative responses appreciably. Derivatives in which alanine in the peptide portion of L4-MDP was replaced by methylalanine or valine failed to induce stimulation. However, the cross-reactivity with BCG was regained in the MTP derivative that was formed by adding lysine to dipeptide containing methylalanine or valine. Whether this cross-reactive pattern was correlated with enhanced induction of tumor immunity was further investigated. According to the established protocol for the augmented induction of tumor immunity, BCG-primed C3H/He mice were immunized with various haptenic MDP-coupled syngeneic X5563 tumor cells. Immunization with tumor cells conjugating BCG-cross-reactive haptens resulted in enhanced tumor immunity, whereas immunization with tumor cells coupling non-cross-reactive haptens failed to produce anti-X5563 tumor immunity. These results indicate that the peptide portion in these haptenic structures is critical in the generation of BCG cross-reactivity leading to enhanced tumor immunity.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1986

Augmentation of antitumor immune response by trinitrophenyl (TNP)-reactive helper T-cells: enhanced induction of tumor-specific Lyt-1+2- T-cell-mediated delayed-type hypersensitivity from spleen cells of tumor-bearing mice by TNP helpers.

Spleen cells from X5563 tumor-bearing syngeneic C3H/HeN mice were stimulated in vitro with trinitrophenyl (TNP)-modified or unmodified X5563 tumor cells. TNP-reactive helper T-cells obtained from TNP-primed C3H/HeN mice were added to the above cultures in an attempt to augment the induction of anti-X5563 delayed-type hypersensitivity (DTH) responses. The DTH responses were measured by adoptive transfer of cultured cells together with unmodified X5563 cells into footpads of syngeneic mice. Cultures of spleen cells from tumor-bearing mice plus X5563 or TNP-modified X5563 cells failed to generate anti-X5563 DTH responses. In contrast, addition of TNP-helper T-cells to the cultures resulted in appreciable DTH as well as in cytotoxic responses to X5563 tumor cells. Demonstration of this immunity was dependent on the presence of TNP-X5563 tumor cells as stimulators during the culture period. The anti-X5563 DTH effector cells augmented by TNP helpers were found to be of the Lyt-1+2- phenotype and were tumor specific, since DTH responses were observed when the cultured cells were injected with X5563 but not when injected with another syngeneic tumor. These results demonstrate that TNP-helper T-cells are capable of augmenting the induction of tumor-specific Lyt-1+2- T-cell-mediated DTH responses from lymphoid cells of tumor-bearing mice upon the stimulation of TNP-reactive tumor cells. The results are discussed in relation to: a previously described tumor-specific immunotherapy model in which a growing tumor regressed by virtue of TNP helpers and the implications of augmenting induction of tumor-specific DTH responses in antitumor resistance.

Animals↗
PubMed1986

Demonstration of intratumoral infiltration of tumor-specific Lyt-1+2- T cells mediating delayed-type hypersensitivity response and in vivo protective immunity.

The present study demonstrates the intratumoral infiltration of lymphocytes mediating anti-tumor delayed-type-hypersensitivity (DTH) responses as well as in vivo protective immunity. The surface phenotype and tumor specificity of these effector lymphocytes were determined. X5563 tumor-infiltrating lymphoid cells were obtained from the tumor mass of syngeneic C3H/HeN mice 2 weeks after the intradermal inoculation of 10(6) viable X5563 tumor cells. These lymphoid cells consisted of Thy-1-positive (29-35%), surface immunoglobulin-positive (16-29%), large granule-positive (15-25%) and esterase-staining-positive (10-20%) cells. They were tested for anti-X5563 DTH responses by utilizing a local adoptive transfer system and for tumor-neutralizing activity in a Winn assay. The results indicate that X5563 tumor-infiltrating lymphoid cells exhibited appreciable anti-X5563 DTH responses and conveyed complete protection against the tumor. Treatment of these lymphoid cells with anti-Thy-1.2 or anti-Lyt antibodies plus complement revealed that the in vivo anti-tumor immune responses were mediated predominantly by a Lyt-1+2- T cell subset. Such Lyt-1+2- T cell-mediated immunity was tumor-specific, since X5563-infiltrating and syngeneic MH134 hepatoma-infiltrating cells exhibited DTH response and tumor-neutralizing activity selectively against the respective tumor cell types. Thus, these results indicate that tumor-specific in vivo-protective Lyt-1+2- T cells infiltrate into the tumor mass. The results are discussed in the context of 1) the interrelation of DTH responses and the tumor protection mediated by the Lyt-1+2- T cell subset and 2) possible cellular interactions between Lyt-1+2- T cells and co-existing nonspecific tumoricidal effector cells such as macrophages.

Animals↗
PubMed1986

The role of I-region associated antigen (Ia)-bearing accessory cells in the generation of cytotoxic T cells in a subpopulation of thymocytes.

The roles of killer-helper factor (KHF) and accessory cells bearing I-region associated antigen (Ia) in the generation of cytotoxic T lymphocytes (CTL) were analyzed. Peanut agglutinin-binding (PNA+) thymocytes from C3H/HeN mice generated efficient CTL responses against 2,4,6-trinitrophenyl (TNP)-modified syngeneic spleen cells in the presence of cell-free supernatant (CFS) derived from purified protein derivatives (PPD)-stimulated Mycobacterium tuberculosis-primed BALB/c spleen cell culture (PPD-CFS). The KHF which is present in PPD-CFS devoid of the activities of IL-1 or IL-2 was required in conjunction with IL-2 for generation of CTL in PNA+ thymocytes. In contrast, PNA- thymocytes as well as spleen cells could generate CTL in the absence of helper factors. However, a significant CTL response against Ia-negative syngeneic tumor cells was not induced from either PNA+, PNA- thymocytes or spleen cells in the absence of Ia-positive accessory cells. Moreover, the treatment of spleen cells with relevant anti-Ia antiserum plus complement before TNP-modification abrogated the stimulatory capacity of TNP-spleen cells. In both cases, the addition of Ia-positive accessory cells restored the impaired capacity of TNP-modified stimulator cells. The addition of IL-1 to the culture of PNA- thymocytes or spleen cells stimulated with TNP-X5563 cells in the absence of accessory cells restored the CTL generation. In contrast, the addition of IL-1 to the culture of PNA+ thymocytes was ineffective. The role of Ia-positive accessory cells in the generation of CTL in a subpopulation of thymocytes is discussed.

Animals↗
PubMed1986

The role of anti-asialo GM1 antibody-sensitive cells in the implementation of tumor-specific T cell-mediated immunity in vivo.

The present study deals with the role of cells sensitive to anti-asialo GM1 antibody treatment in T cell-mediated tumor cell eradication in vivo. Rabbit anti-asialo GM1 antiserum was injected into C3H/He mice. This treatment not only resulted in almost complete abrogation of natural killer (NK) cell activity but also produced a potent inhibiting effect on the generation of activated macrophage activity induced by inoculating Propionibacterium acnes (P. acnes). Such an immunodepressed state lasted for 20 days or more after 5 consecutive injections of anti-asialo GM1 antiserum. These anti-asialo GM1 antibody-treated C3H/He mice were used as recipients in Winn assays, in which the neutralizing activity of spleen cells immunized to syngeneic X5563 tumor cells was assessed. The results demonstrated that anti-X5563 immune spleen cells depleted of asialo GM1-positive cells by the in vitro treatment with anti-asialo GM1 antibody plus complement exhibited potent anti-X5563 tumor-neutralizing activity in antibody-untreated normal recipient mice. In contrast, the X5563-immune spleen cells depleted of asialo GM1+ cells failed to produce tumor protection in asialo GM1 antiserum-treated recipient mice. When T cell-deprived B cell mice were used as recipients in Winn assays, X5563 immune spleen cells depleted of asialo GM1+ cells exhibited or failed to exhibit tumor-neutralizing activity in asialo GM1 antiserum-untreated or -treated recipient B cell mice, respectively. These results indicate that the implementation of T cell-mediated in vivo protective immunity requires the participation of anti-asialo GM1 antibody-sensitive cells, but not necessarily the host's T cells.

Animals↗
PubMed1986

Expression of H-2 antigens and inducibility of antitumor immune responses in various tumor cell clones established from methylcholanthrene-induced fibrosarcomas.

A large number of fibrosarcoma cell lines was established in vitro from a tumor mass induced freshly by inoculating 3-methylcholanthrene (MCA) subcutaneously (sc) into C3H/HeN mice, and more than five clones were isolated from each cell line by the limiting dilution technique. The present study investigated a) qualitative and quantitative comparison of the immunogenicity [tumor-associated transplantation antigen (TATA) activity] of different tumor clones and b) the relationship between such immunogenicity and the expression of H-2 class I antigens. When TATA were compared between different clones from the same tumor, these TATA were revealed to be cross-reactive to each other. On the other hand, the comparison of TATA between clones from different tumors demonstrated the existence of individually unique TATA in these clones. In addition to qualitative heterogeneity of TATA from different tumors, the magnitude of immunogenicity was also heterogeneous in the individual clones established. Whether or not such quantitative heterogeneity of immunogenic strength was related to the expression of H-2 (class I) antigens was examined by flow microfluorometry studies using anti-H-2k antibodies. The results demonstrated that there was no correlation between TATA activity capable of inducing in vivo tumor resistance and the expression of H-2 antigens. This contrasted with parallelism between the expression of H-2 antigens and inducibility of cytotoxic T lymphocytes (CTL) or lysability of tumor cell clones by CTL. These results are discussed in the context of the cellular mechanism of tumor cell eradication in vivo and the regulation of cell surface H-2 expression in vitro and in vivo.

Animals↗
PubMed1986

Requirements of adherent cells for activating Lyt-1+2- T cells as well as for functioning as antitumor effectors activated by factor(s) from Lyt-1+2- T cells.

The mechanism by which tumor-specific Lyt-1+2- T cells exhibit their antitumor effect in collaboration with an adherent cell population was investigated with the use of a double diffusion chamber. The double diffusion chamber was prepared by separating the two chambers from each other by a Millipore membrane and implanted in the peritoneal cavity of C3H/He mice. When one chamber contained normal C3H/He spleen cells plus syngeneic viable MH134 hepatoma cells and the other contained normal C3H/He spleen cells plus syngeneic viable X5563 plasmacytoma cells, tumor cells in both chambers continued to proliferate. In contrast, the injection of spleen cells immunized to the MH134 tumor into one (the first) chamber containing MH134 tumor cells not only resulted in the growth inhibition of MH134 tumor cells, but also exhibited an appreciable inhibitory effect on the growth of X5563 tumor cells admixed with normal spleen cells in the other (second) chamber. The growth inhibition of X5563 tumor cells in the second chamber was mediated by Lyt-1+2- T cells specific for MH134 tumor cells admixed in the first chamber. Such tumor-specific Lyt-1+2- T cell function was dependent on the existence of adherent cells in the first chamber, and adherent cells in the second chamber were also required for the X5563 growth inhibition. In addition, when the second chamber containing adherent cells, instead of the connection to the first chamber, was provided with macrophage-activating factor (MAF), X5563 growth inhibition was also observed. These results indicate that adherent cells are required for activating tumor-specific Lyt-1+2- T cells and for functioning as nonspecific antitumor effector cells activated by factor(s) such as MAF from Lyt-1+2- T cells.

Animals↗
PubMed1986

Comparative studies on B cell reactivities in two X-linked immunodeficient mice to the B cell-stimulating factors.

Responsiveness of B cells from X-linked immunodeficient CBA/N and DBA/2Ha mice to the B cell growth factor-1 (BCGF-I or BSF-1) and B cell differentiation factors (B151-TRF1 and B151-TRF2) was comparatively studied. B cells from CBA/N mice did not respond to BSF-1 in the presence of soluble anti-mu antibody. However, the BSF-1-response of CBA/N B cells was detected when activated by the anti-mu antibody-coupled Sepharose-beads. In the B151-TRF1 assay, antigen-unprimed B cells from CBA/N mice failed to respond to B151-TRF1, whereas antigen-primed B cells became responsive to B151-TRF1. In the B151-TRF2 assay, CBA/N B cells were non-responder to B151-TRF2. In these assays, however, unprimed CBA/N B cells were able to absorb both B151-TRF1- and B151-TRF2-activities to the same extent as the non-defective strain B cells. These results indicate that B cell defect in CBA/N mice may be reflected by some abnormality in signal transmission at encounter to the B cell-stimulating factors but not by inability to bind these factors. These low responder properties of CBA/N B cells were all inherited in an X-linked recessive manner. In contrast, B cells from DBA/2Ha mice well responded to BSF-1 and B151-TRF2, whereas both antigen-unprimed and -primed DBA/2Ha B cells failed to respond to B151-TRF1. This selective B151-TRF1-unresponsiveness of DBA/2Ha B cells was also controlled by an X-linked recessive inheritance. Moreover, in contrast to CBA/N mice, selective unresponsiveness of B cells to B151-TRF1 in DBA/2Ha mice was reflected by the absence of B151-TRF1-receptor expression, as demonstrated by absorption experiment. The B cell populations found in these two distinct X-linked immunodeficient mice may provide an useful experimental model for analyzing B cell activation process mediated by various B cell stimulation factors.

Animals↗
PubMed1986

High plasma cholecystokinin levels in patients with chronic pancreatitis having abdominal pain.

Plasma cholecystokinin (CCK) responses after ingestion of a test meal in patients with mild chronic pancreatitis having abdominal pain were studied with a radioimmunoassay using the CCK specific antiserum (OAL-656) produced by a novel immunization procedure. Mean concentration of the fasting plasma CCK determined using CCK-8 as a standard was 31.5 +/- 5.8 pg/ml in six patients who had mild impaired exocrine function with pain, and was significantly higher than 10 healthy subjects (9.8 +/- 1.8 pg/ml). In those patients, the ingestion of a liquid test meal led to a peak of 75.1 +/- 25.4 pg/ml at 30 min, and the 120-min integrated CCK response (5427 +/- 1217.3 pg X min/ml) was significantly higher than in healthy subjects (1538 +/- 110.1 pg X min/ml).

Abdomen↗
PubMed1985

T-T cell interaction in the in vitro induction of delayed-type hypersensitivity (DTH) responses: demonstration of vaccinia virus-reactive helper T cell activity involved in enhanced induction of DTH responses.

C3H/HeN mice were inoculated i.p. with viable vaccinia virus to generate virus-reactive helper T cell activity. 850R X-irradiated spleen cells from vaccinia virus-primed or unprimed mice as helper cells were stimulated in vitro with either trinitrophenyl (TNP)-modified syngeneic spleen cells (TNP-self), vaccinia virus-infected spleen cells (virus-self), or cells modified with TNP subsequent to virus infection (virus-self-TNP) in the presence of normal C3H/HeN spleen cells (responding cells). After 5 days of culture, effector cells were tested for anti-TNP delayed-type hypersensitivity (DTH) responses by adoptive transfer into footpads of syngeneic C3H/HeN recipient mice together with TNP-self. The results demonstrate that spleen cells from virus-primed mice failed to enhance anti-TNP DTH responses when in vitro stimulation was provided by either virus-self or TNP-self alone. In contrast, spleen cells from vaccinia virus-primed mice, but not from unprimed mice, could augment anti-TNP DTH responses when stimulated by virus-self-TNP. Such a helper activity provided by vaccinia virus-primed mice was shown to be antigen-specific, and mediated by Lyt-1+2-T cells. DTH effector cells enhanced by helper cells were also antigen-specific and Lyt-1+2-T cells. Furthermore, vaccinia virus-reactive helper T cell activity could be applied to augmented induction of anti-tumor DTH responses by stimulation with virus-infected syngeneic fibrosarcoma tumor cells. Thus, these results provide evidence for the role of antigen-specific helper T cells in augmenting the development of DTH responses to cell surface antigens including tumor antigens.

Animals↗
PubMed1985

The augmentation of tumor-specific immunity using haptenic muramyl dipeptide (MDP) derivatives. I. Synthesis of a novel haptenic MDP derivative cross-reactive with Bacillus Calmette Guerin and its application to enhanced induction of tumor immunity.

A new haptenic compound, a muramyl dipeptide (MDP) derivative (designated as L4-MDP-ONB) cross-reactive with Bacillus Calmette Guerin (BCG) was synthesized. The cross-reactivity of L4-MDP hapten to BCG was demonstrated from the following evidence; (a) lymph node cells from BCG-primed C3H/HeN mice exhibited appreciable L4-MDP-specific proliferative responses to the in vitro stimulation of L4-MDP-modified syngeneic cells (L4-MDP-self); (b) inoculation of L4-MDP-self into footpads of BCG-primed C3H/HeN mice elicited ample delayed type-hypersensitivity (DTH) responses in vivo as measured by footpad swelling; and (c) BCG-primed mice contained L4-MDP-reactive helper T cell activity which functions to augment the generation of effector T cell responses to cell surface antigens. This crossreactivity between L4-MDP hapten and BCG as measured by the helper T cell activity was applied to enhanced induction of tumor-specific immunity. When BCG-primed C3H/HeN mice were immunized with L4-MDP-modified syngeneic X5563 tumor cells, these mice could generate augmented tumor-specific in vivo protective (tumor neutralizing) immunity as well as in vitro cytotoxic T cell responses. These results indicate the effectiveness of L4-MDP hapten in augmenting tumor-specific immunity. The present approach is discussed in the context of potential advantages of this new hapten for its future application to clinical tumor systems.

Acetylmuramyl-Alanyl-Isoglutamine↗