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PubMed2004

Assessment of cellular immunity to human cytomegalovirus in recipients of allogeneic stem cell transplants.

Effective reconstitution of cellular immunity following hematopoietic stem cell transplantation (HCT) is thought to be important for protection from the morbidity caused by cytomegalovirus (CMV) reactivation and disease. This review critically discusses current methods for assessment of CMV-specific cellular immune responses, with emphasis on flow cytometry-based methodologies such as MHC-I and MHC-II tetramer staining and intracellular cytokine assays. The advantages and weaknesses of these assays are considered in comparison to traditional immunologic techniques. Application of these newer methodologies has provided insight into the dynamics of the levels of CMV-specific CD4(+) and CD8(+) T-lymphocytes following HCT, and into the sources and diversity of these cells. Data from preliminary clinical studies suggest that CMV-specific CD8(+) T-lymphocyte levels greater than 1 x 10(7)/L of peripheral blood may correlate with protection from CMV disease. Studies on the functional phenotypes of CMV-specific CD8(+) T-lymphocytes such as cytokine production, degranulation, and cytotoxicity have indicated that these cells are heterogeneous with regard to these properties. Future research will focus on establishing whether any of these immunologic assays will serve as a correlate of protection and inform as to which patients are at high risk for CMV reactivation and disease. Identification of an informative assay may allow its incorporation into standard clinical practice for monitoring HCT patients.

CD4-Positive T-Lymphocytes↗
PubMed1993

Cellular immune responsiveness in rabbits with Setaria digitata filarial antigen and TDM adjuvant.

The purified surface antigens of the bovine filarial parasite Setaria digitata were used as an antigen to immunize rabbits. The aqueous suspensions of trehalose 6-6' dimycolate (TDM) has been successfully used as an effective immunomodulator in experimental studies on filariasis. The effectiveness of such an antigen-TDM combination was demonstrated by enhanced humoral and cellular immunity. Administration of antigen alone shows only humoral immunity. The detectable cellular immune responses further confirm the effect of filarial antigen-TDM combination. The cell-mediated immunity was expressed in vivo by delayed skin reaction and in vitro by leukocyte and macrophage migration inhibition tests.

Adjuvants, Immunologic↗
PubMed1977

[Protective effect of cellular immunity in experimental Flavivirus infections].

Experiments were conducted with the tick-borne encephalitis (TE) virus; confirmation of a protective action of cellular immunity in mice was obtained. Administration of sensitized splenocytes to the animals together with the virus was accompanied with an increase of their mean survival or with the reduction of mortality in comparison with control animals given nonimmune or destroyed cells. The protective action of the effector cells was not connected with the intensification of antibody formation in the recipients. A high specificity of cellular immunity was noted in experimental flaviviral infections. The presence of common antigens in the TE and Langat viruses was revealed with the acid of cross splenocyte migration inhibition test (CSMRT). There was also revealed a difference of these viruses from the viruses of yellow fever, Dengue type 2, or Sindbis. The results of studying of the specificity of cellular immunity in the CSMRT found confirmation in experiments with adoptive transfer of splenocytes. Cross protection was caused only by splenocytes sensitized to the TE and Langat viruses.

Animals↗
PubMed2001

Enhanced CD8+ T cell immune response against a V3 loop multi-epitope polypeptide (TAB13) of HIV-1 Env after priming with purified fusion protein and booster with modified vaccinia virus Ankara (MVA-TAB) recombinant: a comparison of humoral and cellular immune responses with the vaccinia virus Western Reserve (WR) vector.

The humoral and cytotoxic T-lymphocyte (CTL) responses have been shown to be determinant in the clearance of many viral infections and because of those characteristics, vaccine candidates against AIDS are designed to enhance both arms of the immune system. While a protocol of immunization able to confer protection in humans against HIV will have to await the results of current clinical trials, it remains important to identify protocols of immunization in animals that achieve significant levels of humoral and cellular immune responses to HIV. In this study we have carried out a comparative analysis of the immune responses elicited in mice immunized with recombinants based on the modified vaccinia virus Ankara strain (rMVA) versus the Western Reserve strain (WR) of vaccinia virus (rVV), both expressing a V3 loop multi-epitopic protein from eight different HIV isolates (TAB13). We found that during priming, rMVA elicited a two- to three-fold higher specific CD8+ T cell response than rVV. Similar enhancement was observed during priming with purified protein TAB13 followed by a booster with rMVA. The epitopes LR150, MN and IIIB, located at the ends and in the middle of the chimeric protein, were able to induce a specific CD8+ T cell response, both after priming or prime/booster with the recombinant viruses but not after prime/booster with TAB13. By examining the cytokine pattern, the immune response triggered by these vectors was of Th-1 type. Humoral immune responses were higher in animals immunized with TAB13/TAB13 or TAB13/rVV than in animals immunized with TAB13/rMVA. These findings demonstrate that during priming or in a prime/booster immunizations, rMVA is superior to rVV in the ability to enhance specific cellular responses to an HIV-1 protein, and that both humoral and cellular immune responses to theV3 loop epitope of HIV-1 Env can be obtained by priming with TAB13 followed by a booster with viral vectors.

AIDS Vaccines↗
PubMedDate not supplied

Cellular immunity delimits adenoviral gene therapy strategies for the treatment of neoplastic diseases.

BACKGROUND: Adenoviral gene therapy is a promising new approach for the treatment of neoplastic diseases. To design rational clinical trials and distinguish the effects of therapeutic transgene expression from those caused by viral infection alone, the immune response to the vector must be understood. In these experiments, we further define cellular immunity to recombinant adenovirus. METHODS: The immune response to hepatic adenoviral gene transfer was studied in infected mice by depleting T cells with an anti-CD3 antibody, measuring splenocyte cytokine production, determining the impact of transgene expression on inflammation, and assessing liver MHC protein expression. RESULTS: The cellular immune response to recombinant adenovirus is (1) averted by T lymphocyte depletion, (2) marked by a TH1 response with increased IL-2 production, (3) directed against both the transgene product and viral proteins, and (4) associated with increased hepatocyte MHC Class I expression. CONCLUSIONS: It is necessary to take into consideration the constraints imposed by the immunogenicity of recombinant adenovirus and its transient transgene expression in the clinical application of adenoviral gene transfer for the treatment of cancer.

Adenoviruses, Human↗
PubMed1986

Modulation of cellular immune responses in mice with disseminated histoplasmosis by recombinant interleukin-2.

Depression of the cellular immune responses in mice with disseminated histoplasmosis is associated with deficient production of interleukin-2 (IL-2) by splenocytes. Therefore, we examined whether a highly purified preparation of IL-2, recombinant human IL-2 (rIL-2), could modify the cellular immune responses in infected mice and whether this lymphokine could alter the severity of histoplasmosis in animals. Exogenous rIL-2, at concentrations of up to 1,000 U/ml, failed to augment the proliferative responses to concanavalin A by unfractionated splenocytes or splenic T cells from mice infected for 1 week. In addition, rIL-2 did not modulate the plaque-forming cell response to sheep erythrocytes by splenocytes from these same mice. However, at week 3, rIL-2 in concentrations ranging from 10 to 1,000 U/ml considerably augmented the proliferative response to concanavalin A and plaque-forming cell response to sheep erythrocytes by splenocytes from infected mice. Kinetics studies demonstrated that rIL-2 exerted maximal immunoregulatory activity when added on day 0 or 1 to cultures of splenocytes. In vivo administration of rIL-2, 200 to 20,000 U/day, for 10 days to normal and 3-week-infected mice did not alter the proliferative activity of splenocytes to concanavalin A; 200,000 U of rIL-2 per day actually depressed the proliferative responses of splenocytes from normal and infected mice. In vivo, rIL-2 did not modify delayed-type hypersensitivity responses to sheep erythrocytes or to histoplasmin by normal and infected mice. Moreover, treatment with rIL-2 in vivo did not reduce the number of Histoplasma CFU in spleens of mice. Thus, despite the immunoenhancing effect of rIL-2 in vitro, this lymphokine failed to exert similar effects in vivo.

Animals↗
PubMed1993

Mucosal and systemic cellular immune responses induced by Toxoplasma gondii antigens in cyst orally infected mice.

This study was performed to determine the T-cellular immune responses following Toxoplasma gondii oral infection and to assess further toxoplasma antigens on their ability to stimulate in vitro mucosal and systemic T-cell immunity. Parasite-specific cellular immune responses in Peyer's patches (PP), in mesenteric lymph nodes (MLN) and in spleen (SPL) were investigated using a lymphoblastic transformation test following oral infection of mice with strain 76K cysts of T. gondii. An early toxoplasma sonicate-induced mucosal T-cell proliferation occurred in MLN and PP with a peak responsiveness on day 6 post-infection (PI) and rapidly reached background levels on day 7 PI in PP and on day 8 PI in mesenteric lymph nodes. A later splenic cellular blastogenesis was observed from day 28 PI and persisted throughout the experiment (day 91). At the time of T-cell proliferation, FACS analyses revealed a decrease in the relative percentages of CD4+ and CD8+ T cells with a predominance of CD8+ lymphocytes which leads to an inversion of the CD4/CD8 ratios. We found that CBA/J is a high responder mouse strain in the induction of mesenteric and splenic T-lymphocyte blastogenesis compared to the intermediate responder BALB/c and low responder C57BL/6. Toxoplasma gondii antigens SAG1 (30,000 MW) and GRA4 (40,000-41,000 MW), which are known to induce locally IgA antibodies, are shown to stimulate primed mucosal T lymphocytes from CBA/J and BALB/c mice whereas no proliferation was demonstrated with C57BL/6 T cells. 229-242 peptide, derived from the deduced amino acid sequence of GRA4, only induces detectable proliferation of primed-CBA/J T lymphocytes. Following oral experimental infection, the in vitro mesenteric response to a toxoplasma sonicate is dominated by a Th2-type cytokine pattern whereas a predominant Th1 cytokine response is observed in the spleen. Finally, in vitro stimulation of mesenteric T cells with the three defined toxoplasma antigens resulted in secretion of interleukin-5 (IL-5) and IL-6 (except for SAG1) and interferon-gamma (IFN-gamma) whereas no detectable IL-2 or IL-4 was observed.

Animals↗
PubMed1997

[Prognostic significance of cellular immunity in surgical treatment of esophageal cancer].

The aim of the study was to investigate the influence of perioperative changes of the cellular immunity parameters on long-term survival following esophagectomy for carcinoma of the esophagus. In 39 patients several immunological parameters have been assessed before and 2 weeks after the operation: WBC, lymphocyte count, lymphocyte T% (E-rosette test), helper/suppressor lymphocyte T subpopulations (teophylline test), NBT test, and in vivo Multitest CMI (skin delayed hypersensitivity for recall antigens). Survival was analyzed using Kaplan-Meier method according to the stage (pTNM, UICC'92) and to the grade of perioperative cellular immunity (pCI) deterioration. Three groups of patients were identified with: 1) improvement or stabilization of pCI (n = 5); 2) deterioration of 1 or 2 pCI parameters (n = 21); and 3) deterioration of 3 or more pCI parameters (n = 13). Follow-up time ranged from 4 to 65 months. Eight patients died in hospital due to postoperative complications, 3 patients are alive (1 of them with Tis alive at 52 months of follow-up), and the remaining patients died during follow-up. Mean survival time of patients in stage II (n = 7), III (n = 17), and IV (n = 14) was 18, 17, and 6 months respectively (p = 0.017, log rank test). Mean survival time of patients in group 1, 2, and 3 was 21, 20, and 5 months respectively (p < 0.001, log rank test). On bivariate survival analysis encountering both factors, stage was found to be the only independent prognostic factor (p = 0.008, Cox regression model). Deterioration of the cellular immunity in the perioperative period is entirely related to the stage of the disease, which is the only independent prognostic factor in carcinoma of the esophagus.

Adenocarcinoma↗
PubMed1992

Replication-defective mutants of herpes simplex virus (HSV) induce cellular immunity and protect against lethal HSV infection.

Live viruses and live virus vaccines induce cellular immunity more readily than do inactivated viruses or purified proteins, but the mechanism by which this process occurs is unknown. A trivial explanation would relate to the ability of live viruses to spread and infect more cells than can inactivated virus. We have used live but replication-defective mutants to investigate this question. Our studies indicate that the immune responses of mice to live virus differ greatly from the responses to inactivated virus even when the virus does not complete a replicative cycle. Further, these studies indicate that herpes simplex virus-specific T-cell responses can be generated by infection with replication-defective mutant viruses. These data indicate that the magnitude of the cellular immunity to herpes simplex virus may be proportional to the number or quantity of different viral gene products expressed by an immunizing virus.

Animals↗
PubMed2004

Effect of hypertonic saline infusion on postoperative cellular immune function: a randomized controlled clinical trial.

BACKGROUND: Previous studies found hypertonicity to affect immune responses in intact laboratory animals and in human blood cell cultures. In this study, the authors investigated the cellular immune response to surgery after preoperative infusion of hypertonic saline in humans. METHODS: Sixty-two women scheduled to undergo abdominal hysterectomy were randomly assigned to single-blinded infusion of 4 ml/kg NaCl, 7.5%; 4 ml/kg NaCl, 0.9%; or 32 ml/kg NaCl, 0.9%, over 20 min. Blood was collected at baseline, during surgery, and 1, 24, and 48 h after surgery for the determination of leukocyte and differential counts, flow cytometric phenotyping of mononuclear cells, and natural killer cell activity against K 562 tumor cells. Phytohemagglutinin-induced lymphocyte proliferation, plasma elastase, and neutrophil chemotaxis were measured at the same time points except during surgery. The authors tested cell-mediated immune function in vivo by delayed-type hypersensitivity reaction in the skin. RESULTS: Surgery induced well-known changes in the cellular immune response, which were unrelated to the tonicity or volume of the infused fluids. CONCLUSION: Infusion of a clinically relevant dose of hypertonic saline did not seem to modify the postoperative cellular immune response after elective abdominal hysterectomy.

Adult↗
PubMed1996

The role of cyclic AMP and oxygen intermediates in the inhibition of cellular immunity in cancer.

Cell-mediated immunity is often impaired in cancer. This may be partly due to increased amounts of prostaglandin E2 (PGE2) and histamine in the blood of cancer patients, since PGE2 and histamine possess inhibitory effects on cellular immunity. These effects are mediated by cyclic AMP (cAMP), which is increased in leukocytes by PGE2 through EP2 and by histamine through H2 receptors and also by epinephrine through beta 2-adrenergic receptors. Increased cAMP activates protein kinase A, which inhibits the formation of interleukin 2 (IL-2) in T cells. The formation of interferon gamma is concomitantly decreased, and cellular immunity is attenuated. In monocyte/macrophages the formation of IL-1 beta, IL-12 and tumor necrosis factor alpha is decreased by cAMP or through the increased formation of IL-10, which is up-regulated by cAMP. This attenuates cellular immunity. In monocytes histamine may decrease the formation of oxygen intermediates, which can induce apoptosis of natural killer cells and thus inhibit immunity. The superoxide anion is a potent inducer of the cyclooxygenase-2 enzyme, which is upregulated in colorectal cancer. Cyclooxygenase-2 catalyzes the formation of PGE2, e.g. in cancer cells. Thus the inhibition of cellular immunity in cancer may be at least partly mediated by cAMP and oxygen intermediates. This may offer new options for cancer immunotherapy.

Cyclic AMP↗
PubMed1977

[Congenital deficiency of humoral and cellular immunity].

The study involves 10 children with primary immunologic deficiency of the humoral and cellular immunity diagnosed on the basis of the clinical symptoms of the disease and immunologic investigation. In 7 children, out of whome three were infants, suffering of recurrent respiratory tract infections, examinations revealed either absence or deficiency of the IgA in the serum and saliva. 2 children presented a classical picture of the Wiskott-Aldrich's syndrome followed by eczema, recurrent infections and trombocytopenia. Having studied the immunologic status in these two children in vitro and in vivo, the authors established deficiency in the humoral and cellular immunity. In an infant aged three months, with diagnosed histiocytosis X after histologic examination of the skin, the authors had examined the function of the T and B cells after which it was concluded that it was a case of rare form of the combined primary immunodeficiency.

Child↗
PubMed1999

Human herpesvirus 8 cellular immune responses in homosexual men.

Little is known about cellular immunity to human herpesvirus 8 (HHV-8), the virus associated with Kaposi's sarcoma (KS). T cell proliferative responses to purified HHV-8 were measured in homosexual men, a group with elevated HHV-8 seroprevalence and high risk of KS. None of 20 blood donor controls had T cell responses to HHV-8. Among human immunodeficiency virus (HIV)-negative homosexual men, 8 (42%) of 19 HHV-8 seropositive men responded as did 4 (16%) of 25 HHV-8 seronegative men. Among HIV-positive homosexual men, however, none of 21 HHV-8 seropositives had T cell responses to HHV-8, even though most responded to common recall antigens, and 10 had >/=400 CD4 cells/mm3. The results suggest that HHV-8 T cell proliferative responses are common in HIV-negative homosexual men and that HIV infection may be associated with diminished HHV-8 cellular immunity, possibly before there is substantial depletion of CD4 cells. If correct, this could explain why KS occurs relatively early in HIV infection/AIDS.

Antibodies, Viral↗
PubMed1980

Dimethyl dioctadecyl ammoniumbromide as an adjuvant for delayed type hypersensitivity and cellular immunity against Semliki Forest virus in mice.

Intracutaneous immunization of BALB/c mice with inactivated Semliki Forest virus mixed with the cationic, surface active lipid dimethyl dioctadecyl ammoniumbromide produced a strong enhancement of delayed type hypersensitivity without detectable antibodies in serum. Furthermore these mice were more protected against intraperitoneal challenge than normal immunized mice. This protection might be explained by an enhancement of cellular immunity against Semliki Forest virus. Dimethyl dioctadecyl ammoniumbromide by itself has no effect on footpad swelling, mortality and mean survival time.

Adjuvants, Immunologic↗
PubMed2004

The impact of different intensities of regular donor plasmapheresis on humoral and cellular immunity, red cell and iron metabolism, and cardiovascular risk markers.

BACKGROUND AND OBJECTIVES: Major studies are still lacking on the impact of differing intensities of long-term donor plasmapheresis, not only on total serum protein, albumin and immunoglobulin G (IgG), but also on humoral and cellular immunity, red cell and iron metabolism, and biochemical cardiovascular risk markers. MATERIALS AND METHODS: Three groups of donors, comprising 483 individuals undergoing differing intensities of long-term serial plasmapheresis, were entered into a cross-sectional study. A fourth control group consisted of 100 non-donors. In addition to measuring total protein, albumin and IgG levels, we determined parameters of humoral and cellular immunity, red cell and iron metabolism and recognized biochemical cardiovascular risk factors. RESULTS: The median annual net amount of plasma donated by the three donor groups was 37, 16 and 10 l, respectively (P < 0.0001). Donors had significantly lower total serum protein, albumin and IgG levels than non-donors (P < 0.0001), but the intensity of plasmapheresis had no influence on those parameters. Like non-donors, all plasma donors had normal humoral and cellular immunity. No increased rates of iron store depletion were observed in the three groups of plasma donors. Plasma donors were not at increased cardiovascular risk. CONCLUSIONS: Regular donor plasmapheresis of up to 45 l of plasma per year appears to be as safe as more moderate plasmapheresis programmes, with respect to the parameters analysed in this study. Individuals donating under these conditions did not develop impaired humoral and cellular immunity, iron store depletion, or increased cardiovascular risk with regard to established biochemical risk markers. Prospective studies are required to determine more exactly than in retrospective analyses the reasons why donors withdraw from plasmapheresis programmes.

Adult↗
PubMedDate not supplied

Humoral and cellular immunity in chronic urticaria.

In chronic recurrent urticaria of months' or years' duration, it is difficult to identify the causative factor. From an immunological point of view, various authors have attempted to demonstrate alterations in levels of immunoglobulins and complement fractions. We do not know of any previous studies of cellular immunity in this disorder. Fifty-one patients with chronic urticaria were studied, 22 females and 29 males, with ages ranging from 8 to 70 years. The patients were considered to be affected by recurrent or chronic urticaria with no clear allergic etiology. In all subjects a determination was made of serum levels of immunoglobulins G, A, M and E and of the complement fractions: C1 inhibitor, C1q, C3, C4 and C5. In addition, a study of cellular immunity was carried out on these patients. The results of tests of humoral immunity in the group of chronic urticarial patients studied showed only an increase of IgM in 41.7%. No significant changes were noted among the complement fractions. The study of cellular immunity gave normal figures for total and for B and T lymphocytes. The only finding which may be worthy of is a slight decrease in active T lymphocytes. The lymphocyte transformation test also gave a normal response to PHA and overall a normal cellular immunity was shown in these patients. At present we do not consider that the increased IgM in 40 to 45% of the cases has any pathogenic diagnostic value.

Adolescent↗