Dental visiting behaviours among primary schoolchildren: Application of the health belief model.

OBJECTIVES: This study aimed to develop and validate a new instrument based on the health belief model and to use the instrument to investigate the determinants of regular dental attendance among primary schoolchildren. METHODS: A cross-sectional study was conducted using a newly developed measurement scale based on the HBM, 4 health-promoting schools participated in the study and 958 students studying in grades 4-6 completed the questionnaire. The psychometric properties of the instrument were analysed, and a path analysis model was used to identify the determinants of regular dental attendance. RESULTS: The instrument had good internal consistency (Cronbach's α = 0.826-0.925) and a factor structure identical to HBM. Overall, the schoolchildren's health beliefs on caries treatment were positive. The determinants of regular dental visit were school location (ß = -0.13), mother's education level (ß = 0.15), susceptibility (ß = -0.18) and barriers (ß = -0.11). CONCLUSION: This study provided evidence that HBM is applicable to children's dental visiting behaviour and their health beliefs towards adherence to caries treatment. Although children had a positive attitude towards dental visits, environmental obstacles would interfere with dental visits. The newly developed instrument could be used to identify high-risk children and help design oral health interventions for these children. Moreover, policy makers should increase the accessibility of dental resources to enhance the utilization of dental care among schoolchildren.

How does graphene grow on complex 3D morphologies?

The growth of two-dimensional materials into three-dimensional geometries holds the promise for high performance hybrid materials and novel architectures. The synthesis of such structures, however, proceeds in fundamentally different flow regimes compared to conventional CVD where pressure differences and wall collisions are neglected. We here demonstrate the remarkable stability of graphene growth under varying fluid dynamic flow regimes. We investigate the growth process across different flow conditions using confined growth in refractory pores. Analysis of the growth rate reveals a transport-limited process which allows experimental determination of the gas diffusion coefficient. The diffusion coefficient was found to be constant for large pore dimension but scales with pore dimension as the pore size decreases below the mean free path providing clear evidence for previously predicted Knudsen molecular-flow conditions for atomic confinement. Surprisingly, changes to the flow conditions by two orders of magnitude do not cause qualitative changes of the graphene growth process. This unique behavior was attributed to rarefied flow conditions by scaling analysis and an analytical relation between growth rate and constriction could be extracted that proves accurate throughout the investigated conditions. Our results demonstrate a fundamentally different growth process compared to traditional CVD processes that is akin to atomic layer deposition and highlight the feasibility of high-quality 2D-material growth on 3D morphologies with ultra-high aspect ratios.

Oral health disparities of children among Southeast Asian immigrant women in arranged transnational marriages in Taiwan.

This study assessed the oral health disparities and oral health care needs of children whose parents are Southeast Asian immigrant women in arranged transnational marriages. We used the baseline data of the Lay Health Advisor Approach to Promote Oral Health Program (LHA-POHP) to explore the disparities in oral health between immigrant and native children, and the factors associated with their oral health. A cross-sectional community-based study was conducted to collect data from mothers and their preschool children in Southern Taiwan in 2011. A total of 590 (440 natives, 150 immigrants) children aged 4-6 years and their mothers completed the questionnaire and oral examination. Multiple regression models were used to analyze the association between children's oral health and their related factors. The caries index was 6.05 in immigrant children and 3.88 in native children (p < 0.001). The caries prevalence of maxillary anterior teeth in the labial surfaces was higher among immigrants, ranging from 14.7 to 22%. The factor associated with children's caries index was maternal tooth brushing frequency (adjusted odds ratio [aOR] = 8.95, 95% confidence interval [CI] 1.95-41.05). When the mothers did not direct children to brush teeth after eating sweets, their children were more likely to have decayed teeth (aOR = 3.54, 95% CI 1.04-12.03). Children's filled teeth were related to their dental regular check-ups (aOR = 2.28, 95% CI 1.26-4.10). Disparities in oral health among immigrant and native children were observed. The findings suggest that culturally adequate oral health promotion intervention programs should be implemented for immigrants.

Antimicrobial photodynamic therapy using a diode laser with a potential new photosensitizer, indocyanine green-loaded nanospheres, may be effective for the clearance of Porphyromonas gingivalis.

BACKGROUND: Antimicrobial photodynamic therapy (aPDT) is a new treatment method for the removal of infectious pathogens using a photosensitizer and light of a specific wavelength, e.g., toluidine blue with a wavelength of about 600 nm. We explored a new photosensitizer and focused on indocyanine green (ICG), which has high absorption at a wavelength of 800-805 nm. We investigated the bactericidal effect of PDT on Porphyromonas gingivalis using a new photosensitizer, ICG-loaded nanospheres with an 805 nm wavelength low-level diode laser irradiation. METHODS: We designed ICG-loaded nanospheres coated with chitosan (ICG-Nano/c) as a photosensitizer. A solution containing Porphyromonas gingivalis (10(8)  CFU/mL) with or without ICG-Nano/c (or ICG) was prepared and irradiated with a diode laser or without laser irradiation as a negative control. The irradiation settings were 0.5 W with a duty ratio of 10%, for 3-100 ms in repeated pulse (RPT) or continuous wave mode. CFU were counted after 7 d of anaerobic culture. RESULTS: We observed that ICG-Nano/c could adhere to the surface of P. gingivalis. When ICG-Nano/c was used for aPDT, irradiation with RPT 100 ms mode gave the lowest increase in temperature. Laser irradiation with ICG-Nano/c significantly reduced the number of P. gingivalis (i.e., approximately 2-log10 bacterial killing). The greatest bactericidal effect was found in the RPT 100 ms group. However, laser irradiation (RPT 100 ms) with ICG, as well as without photosensitizer, had no effect on the number of bacteria. CONCLUSIONS: Within the limits of this study, ICG-Nano/c with low-level diode laser (0.5 W; 805 nm) irradiation showed an aPDT-like effect, which might be useful for a potential photodynamic periodontal therapy.

Host control of tumor growth.

A humoral factor (molecular weight less than 60,000) that was present in the ascitic fluid of mice bearing intraperitoneal tumors and in pleural effusions from human cancer patients was found to promote the growth of a murine tumor and to suppress cell-mediated tumor immunity. However, the hosts that had recovered from the immunosuppressive state produced a serum factor that could neutralize the immunosuppressive effect.

Minimally invasive approaches to treating chemosis of the eyes from unusual dural arteriovenous fistulae.

Chemosis of the eyes is usually attributed to carotid cavernous sinus dural arteriovenous fistulae. Herein, we reviewed unusual cases in which chemosis of the eyes originated from dural ateriovenous fistulae (dAVFs) that were distinctly different from carotid cavernous sinus fistulae. Cases in which ocular symptoms were related to increased intracranial pressure either due to sinus thrombosis or cortical venous drainage without involvement of superior or inferior ophthalmic veins were excluded in this review. Several different types of dural AVFs were associated with chemosis, and these included dAVFs harboring a feeding artery from branches of the external carotid artery directly draining to the superior ophthalmic vein or cavernous sinus via the superior petrous sinus, posterior fossa dAVFs draining via the inferior petrous sinus and cavernous sinus to the ophthalmic vein, a fistula between the ophthalmic artery or branches of the internal carotid artery and inferior ophthalmic vein, or tentorial fistula with a drainage vein to the cavernous sinus via the vein of Galen. This study reviews the symptomatology, treatment options, and cerebrovascular abnormalities observed for these unusual dAVF's with chemosis.

Afferent and efferent interference of cell-mediated cytotoxic reactions by heparin.

Heparin influenced the induction (afferent interference) and effector (efferent interference) phases of cell-mediated cytotoxic reactions against FBL-3 cells, a syngeneic Friend virus-induced leukemia in inbred C57BL/6 mice. Heparin was cytotoxic at high concentrations (greater than or equal to 100 U/ml) and inhibitory for cell-mediated cytotoxic response at lower concentrations (less than or equal to 50 U/ml).

Studies of the mechanisms for the induction of in vivo tumor immunity. II. Distribution and homing of cytotoxic effector and precursor cells.

Cytotoxic T (thymus)-lymphocytes (CTL) with specific cytotoxicity against the leukemia-associated antigens of FBL-3, a syngeneic Friend virus-induced leukemia in C57BL/6 mice, could be adoptively transferred to sublethally X-irradiated (350 R) syngeneic hosts and could be induced by adoptive transfer of either normal or presensitized lymphocytes obtained from immunocompetent hosts. The CTL and their precursor cells were systemically distributed in peripheral lymph nodes and spleen, although they had the tendency of homing to the lymphoid tissue of the same origin. Direct cytotoxicity was obtained with the lymphocytes from these lymphoid tissues, and cells obtained from these lymphoid tissues could produce secondary cytotoxic responses by the mixed lymphocyte tumor cell culture reactions 40--60 days after adoptive transfer. In addition, lymph node and spleen cells had a synergistic effect on the induction of cytotoxicity. These findings indicated that tumor immunity was widely distributed and that various populations of lymphocytes were involved in the generation of efficient cell-mediated cytotoxic responses.

Humoral antibody response and tumor transplantation resistance elicited by fetal tissues in mice.

Immune responses to fetal antigen immunization were studied in C57BL/6 (B6), C3H/HeN (C3H), and BALB/c (BALB) mice. In tests by the isotopic antiglobulin technique, the mice could be grouped in three classes according to their antibody responses: good responders (B6), poor responders (C3H), and nonresponders (BALB). In tumor transplantation experiments, protection against syngeneic tumor-cell challenge, after fetal tissue immunization, was observed only with B6 mice. In addition, experiments on B6 mice showed that resistance to tumor challenge after fetal tissue immunization depended on the quantitative expression of fetal antigens by the tumor cells. Our results indicated that, in addition to other well-known factors, the effectiveness of fetal tissue immunization in tumor-challenge resistance depended on both host responsiveness and the amount of fetal antigen expressed by the tumor cells.

Increased susceptibility to tumor cell immunosuppressive effect in tumor-bearing mice.

Compared to normal hosts, tumor-bearing BALB/c mice were more susceptible to the immunosuppressive effect of tumor cells. At least a tenfold increase was found in the susceptibility mediated by a population of radioresistant spleen adherent cells (AC). The experiments were performed by the study of the suppressive effect of tumor cells on the generation of cytotoxic T-cells in allogeneic mixed lymphocyte culture reactions and allogeneic mixed lymphocyte tumor cell culture reactions. Fewer tumor cells were needed to suppress the T-cell-mediated cytotoxic responses of tumor bearers compared to normal hosts. A normal spleen population could be made to react like the tumor-bearing host by first depletion of its normal macrophages and then reconstitution with spleen AC from tumor bearers. Conversely, reconstitution of the macrophage-depleted tumor bearer's spleen with normal spleen AC made the tumor bearer react like the normal host. Furthermore, tumor cells were needed to trigger the spleen AC of the tumor bearer to fully exert their effect.

Tumor cell-triggered macrophage-mediated suppression of the T-cell cytotoxic response to tumor-associated antigens. I. Characterization of the cell components for induction of suppression.

A tumor cell-triggered macrophage-mediated suppressor mechanism was demonstrated. It suppressed the induction of specific tumor immunity in the syngeneic, primary mixed lymphocyte tumor cell culture reactions. Preexposure of splenic adherent cells (SAC) to syngeneic FBL-3 tumor cells induced complete suppression of the generation of cytotoxic T-cells. The SAC responsible for inducing suppression were consistent with being macrophages. They were resistant to the treatment of anti-Thy-1.2 antibody plus complement and were relatively radioresistant (at least less than or equal to 750 R X-radiation). Adherent cells obtained from lymph nodes or thymuses acted in the same way as SAC. However, preexposure of peritoneal adherent cells to tumor cells failed to induce suppression. In contrast, the simultaneous presence of peritoneal adherent cells with SAC upon exposure to tumor cells prevented the induction of suppression. These peritoneal cells were also consistent with being macrophages. These results confirmed our previous observations obtained with experiments performed in the allogeneic system. An immunoregulatory circuit existed between two subsets of macrophages that were derived from the population of cells in the peritoneal cavity and from spleen, lymph nodes, or thymus. In the presence of tumor cells, these macrophages produced both positive regulation and negative regulation of the T-cell-mediated cytotoxic response against syngeneic tumor cells. The tumor cells may have utilized the host's own immune network to activate the suppressor mechanisms, thus successfully evading the host's immune surveillance.

Tumor cell-triggered macrophage-mediated suppression of the T-cell cytotoxic response to tumor-associated antigens. II. Mechanisms for induction of suppression.

The mechanisms were investigated for the tumor cell-triggered macrophage-induced suppression of T-cell-mediated tumor immunity. Interaction between tumor cells and macrophages triggered the production of prostaglandin(s) (PG) that initiated the suppressor events. In our experiments, PGE1 or PGE2 suppressed the generation of cytotoxic T-lymphocytes in the syngeneic mixed lymphocyte tumor cell cultures. Indomethacin, a PG synthetase inhibitor, blocked the induction of the macrophage-mediated suppression, which suggested that suppression was caused by endogenous PG. This suppression might be further mediated by the generation of suppressor T-cells. Significant reduction in the levels of macrophage-induced suppression was seen in hosts receiving cyclophosphamide treatment, which could eliminate the precursors of suppressor T-cells. These findings indicated that tumor cells may trigger a chain of reactions, through the generation of suppressor factors or suppressor cells, to subvert the host's immune surveillance.

In vitro inhibition of cell-mediated cytotoxicity against syngeneic Friend virus-induced leukemia by immunoregulatory alpha globulin.

Immunoregulatory alpha-globulin (IRA) derived from normal human plasma decreased cytotoxic reactivity as measured by an in vitro 5-iodo-2'-deoxyridine release assay of immune mouse lymphocytes against the syngeneic Friend virus-induced leukemia, FBL-3. This inhibitory effect depended on the dose of IRA used and was not due to the cytotoxic effects of IRA on the effector cells or target tumor cells. We also found elevated levels of serum alpha-gloubins in FBL-3 tumor-bearing mice as compared to normal mice. These data and the demonstration of decreased specific cytotoxic reactivity in FBL-3 tumor-bearing mice suggest that IRA functions in the suppression of the host's immune response against tumors.

Comparison of three isotopic assays of cell-mediated cytotoxicity against mouse tumor cells. I. Basic parameters: baseline controls, target cells, and methods of calculation.

We compared three ddifferent isotopic assays of cell-mediated cytotoxicity under identical test conditions: 51Cr, 125iododeoxyuridine, and [3H]proline release assays. We made these comparisons both in a syngeneic mouse tumor system and an allogeneic system. It was found that several parameters could affect considerably the results obtained with these tests, such as: baseline controls, preparation of target cells, and methods of calculation. In comparison of three different baseline controls, the normal control gave the most consistent results, whereas the other two controls (autologous and medium controls) gave varying results depending upon the condition of the target cells. For use as target cells, established tissue culture cells were usually superior because of a much lower spontaneous release of the isotope, when compared to fresh ascites tumor cells or short-term tissue culture cells. The advantage of established culture cells was particularly noted in isotopic assays with prolonged incubation (20-40 hr). In addition, the methods used for calculation were also shown to affect the apparent outcome of the results.

Comparison of three isotopic assays of cell-mediated cytotoxicity against mouse tumor cells. II. Sensitivity and specificity of the assays and characteristics of effector and sensitizing cells.

Three assays of cell-mediated cytotoxicity in mice, involving release of either 51Cr (CRA), 125iododeoxyuridine (IRA), or [3H]proline (PRA), were compared under identical test conditions. Experiments were performed with effector cells from mice immunized with FBL-3 tumor cells, a syngeneic Friend virus-induced leukemia, or with allogeneic normal spleen cells. With established tissue culture cells as targets, similar results were obtained in all three assays. The cytotoxicity produced by cells from in vivo-immunized mice and the induction of cytotoxicity in vitro were T-cell-dependent. When short-term culture target cells were used, the IRA gave a more selective pattern of cytotoxicity than did the other two assays. However, when remaining target cells at the end of the assay were treated with trypsin, higher levels of 125iododeoxyuridine (125IUDR) release were seen, and the results were then comparable to those in the CRA and PRA. These results indicated that 125IUDR, a nuclear label, could only be released after lysis of cells. In contrast, 51Cr or [3H]proline, which are cytoplasmic labels, could also be released from damaged but unlysed cells. These fundamental differences could give different results in these assays, which could determine their correlation with in vivo transplantation immunity.

Humoral regulation of cell-mediated immunity to syngeneic tumor.

Inoculation i.p. of C57BL/6 mice with FBL-3 cells, a syngeneic Friend virus-induced leukemia, results in progressive growth of ascitic tumors; in contrast, s.c. inoculation of FBL-3 cells produces transient, localized tumor growth; the recipients are then subsequently resistant to further i.p. challenge of this tumor. Experiments were performed to study the effects of humoral factors that might be present in the ascitic fluid and that could affect the growth of the tumors and the host immune response. It was found that ascitic fluids obtained from various murine tumors could indeed promote the s.c. growth of FBL-3 cells. Furthermore, administration of these ascitic fluids was found to suppress the induction of both the primary and secondary cell-mediated cytotoxic responses to FBL-3 cells in vivo and in vitro and to inhibit the effector phase of these cell-mediated cytotoxic reactions in vitro. These studies indicate that the ascitic fluids obtained from tumor-bearing hosts contain humoral factors that can promote tumor growth and suppress immune responses.

Lymphokine-induced cytotoxicity: characterization of effectors, precursors, and regulatory ancillary cells.

In the present study, we have characterized the effectors, precursors, and regulatory ancillary cells involved in the in vitro generation of lymphokine-induced cytotoxicity. It was first shown that at least two lymphokines are needed for the generation of lymphokine-induced cytotoxicity. They are interleukin 2 and a novel lymphokine, the cytotoxic cell differentiation factor (CCDF). CCDF was produced primarily by the macrophages. The effectors of the lymphokine-induced cytotoxic cells thus generated selectively killed tumor targets of different etiological origins. The serological phenotype of lymphokine-induced cytotoxic cell effectors were found to be Thy 1+, Lyt 2-, and AGM1-; therefore, they were neither classic natural killer (NK) cells nor cytotoxic T-lymphocytes. Extensive characterization of the precursors by sequential column separation and antibody lysis and also by limiting dilution analysis showed that they were AGM1+ and Lyt 2-; thus they were NK-like cells. In addition to NK-like cells being identified as the precursors, two other cell compartments were identified as ancillary cells which regulate the lymphokine-induced cytotoxicity. They were the macrophages and T-cells. Macrophages were needed to produce CCDF and to activate the Lyt 1+ helper T-cells to produce interleukin 2. The Lyt 2+ T-cells play a negative role in the regulation of the lymphokine-induced cytotoxic cell response. The process of lymphokine-induced cytotoxicity thus involves a complex interaction between at least two lymphokines (interleukin 2 and CCDF) and three cell compartments, namely, NK-like cells, macrophages, and T-cells of Lyt 1+ and Lyt 2+ phenotypes.

In vivo antitumor activity of anti-CD3-induced activated killer cells.

This study investigates the potential of the alpha CD3-induced killer cells for use in adoptive immunotherapy of tumor growth. The alpha CD3-induced, activated, killer cells (CD3-AK) were generated in DBA/2 (H-2d) splenocytes by preactivation with alpha CD3 and were then cultured in the presence (CD3-AK [alpha CD3+]) or absence (CD3-AK [alpha CD3-]) of alpha CD3. The conventional lymphokine-activated killer (LAK) cells were induced by culturing DBA/2 splenocytes with purified human recombinant interleukin 2. Testing their in vitro cytotoxicity against syngeneic mastocytoma P815, CD3-AK (alpha CD3+) cells gave the highest levels of cytotoxicity and were 20-fold higher than LAK cells and 200-fold higher than CD3-AK (alpha CD3-) cells. However, the cytotoxic activity of LAK or CD3-AK (alpha CD3-) cells was augmented by preincubating them with alpha CD3 for 3 h; then, the difference in cytotoxic activity was reduced from 20- to 4-fold and from 200- to 2-fold, respectively. The in vivo antitumor activity of these killer cells paralleled the in vitro activity. In tests using tumor neutralization experiments, 80-100% of the mice that were challenged with 1 x 10(2) P815 cells remained tumor free after receiving 5 x 10(6) CD3-AK (alpha CD3+) cells. When the challenge dose increased to 1 x 10(3) and to 1 x 10(4) cells, giving CD3-AK (alpha CD3+) cells slowed down the rate of tumor growth but only 20% of the mice remained tumor free. The untreated LAK cells or CD3-AK (alpha CD3-) cells did not induce any protection. After preincubation with alpha CD3 for 3 h, the CD3-AK (alpha CD3-) cells provided protection in 30% of the challenged mice. The phenotype of effectors for mediating the in vitro and in vivo antitumor activities was found to be Thy1+, CD4-, and CD8+ cells. Flow microfluorometry analysis showed that the higher levels of cytotoxic activity obtained with CD3-AK (alpha CD3+) cells could not be simply explained by the increase of CD8+ cells, and the cytotoxic activity of individual CD3-AK (alpha CD3+) cells appeared to be much higher than that of the LAK cells. After tumor growth was established for 1-2 days, giving CD3-AK (alpha CD3+) cells slowed down the rate of tumor growth, and 20% of the mice remained tumor free. These results indicate that CD3-AK cells may be used in the immunotherapy of tumor growth.(ABSTRACT TRUNCATED AT 400 WORDS)

Cell-mediated immunity to leukemia virus- and tumor-associated antigens in mice.

Cell-mediated immune reactions appear to play an important role in resistance against growth of leukemia cells in mice. Possible mechanisms for in vivo protection in two tumor systems are discussed. These tumor models, which are a Friend leukemia virus-induced transplantable tumor, FBL-3, and primary murine sarcoma virus (MSV) -induced tumors, are strongly antigenic; under some conditions, tumors regress completely. In mice with regressing FBL-3 tumors, cell-mediated cytotoxicity was measured by release of [125I]iododeoxyuridine. The response was biphasic, with an initial peak at 10 days and a 2nd peak after 30 days. A boost in reactivity could be elicited by later challenge with tumor cells. All of the reactivity was dependent on T-cells, being eliminated by treatment with anti-theta plus complement. The specificity of the reactions was not completely defined, but it was consistent with Friend type-specific antigen plus broader, common antigens. In mice with regressing MSV tumors, strong cell-mediated cytotoxicity, measured mainly by release of 51Cr, was seen against RBL-5, a Rauscher virus-induced leukemia. A single peak of response occurred at about 14 days after virus inoculation. Upon later challenge with RBL-5 cells, a vigorous and rapid secondary response was elicited, mainly in the region of tumor challenge. This cytotoxic reactivity and in vivo resistance to leukemia.lso was completely dependent on T-cells. In addition, macrophage-mediated inhibition of leukemia cell growth in vitro was seen in this system at the time of peak tumor development. The 51Cr release cytotoxicity was specific and directed primarily against an antigen, MEV-SA1, associated with mouse endogenous C-type viruses. The macrophage-induced growth inhibition appeared to be nonspecific. In both the FBL-3 and MSV tumor systems, protection against tumor growth could be adoptively transferred by immune lymphoid cells. In addition to induction of cell-mediated immunity by tumor cell or virus inoculation, cell-mediated cytotoxic reactivity was found to occur naturally in most young mice. This natural killer activity was quite distinct from the experimentally elicited reactions, being mediated by N-cells, a subpopulation of lymphoid cells with no clearly identifiable cell surface markers. The natural cytotoxicity was also directed against antigenic specificities different from those recognized by the MSV-immune cells. The central issue in all of these studies has been to determine the relationships between the in vitro-detected cell-mediated reactivity and in vivo resistance to leukemia.

Restoration of cytotoxic T lymphocyte function in malignant pleural effusion: interleukin-15 vs. interleukin-2.

The present study attempts to define the role of interleukin-15 (IL-15), as compared with IL-2, in generating cytotoxic T lymphocytes (CTL) from the malignant effusions of cancer patients. Effusion-associated lymphocytes (EAL) from malignant effusion were incubated with IL-15 or IL-2 with or without alphaCD3. Proliferation and cytotoxicity assays were performed. IL-15 was found to have at least an equivalent, if not higher, activity to IL-2 in terms of lymphocyte proliferation and generation of CTL from EAL. The proliferative response of EAL, cocultured with IL-15, with or without alphaCD3, was partly inhibited by pretreatment with an anti-IL2 receptor beta chain monoclonal antibody (mAb). The proliferative response of EAL, cocultured with alphaCD3, IL-2, or both, was partly inhibited by pretreatment with an anti-IL-2 receptor alpha chain mAb. Overnight [5lCr] release assays against K562, Daudi, and the patients' autologous tumor cells were done to evaluate EAL's cytolytic activity. MHC class I Ab blocked the stimulated cytolytic activity of EAL against autologous tumors. An mAb depletion assay showed that the phenotype of the restored EAL was CD16-CD4-CD8+; thus, the restored activity of EAL was CTL activity. The results suggest that both IL-15 and IL-2 can restore CTL activity from EAL in the presence of T cell receptor (TCR)-CD3 engagement, but the effect of IL-15 was superior.