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Immunol Cell Biol. 2002 Dec;80(6):567-73.
The role of CD4+CD25+ immunoregulatory T cells in the induction of autoimmune gastritis.

Laurie KL, Van Driel IR, Gleeson PA.

The Russell Grimwade School of Biochemistry and Molecular Biology, The University of Melbourne, Victoria, Australia.

A number of experimental models of organ-specific autoimmunity involve a period of peripheral lymphopenia prior to disease onset. There is now considerable evidence that the development of autoimmune disease in these models is due to the absence of CD4+CD25+ regulatory T cells. However, the role of CD4+CD25+ regulatory T cells in the prevention of autoimmune disease in normal individuals has not been defined. Here we have assessed the affect of depletion of CD4+CD25+ regulatory T cells in BALB/c mice on the induction of autoimmune gastritis. The CD4+CD25+ T cell population was reduced to 95% of the original population in adult thymectomized mice by treatment with anti-CD25 mAb. By 48 days after the anti-CD25 treatment, the CD4+CD25+ regulatory T cell population had returned to a normal level. Treatment of thymectomized adult mice for up to 4 weeks with anti-CD25 mAb did not result in the development of autoimmune gastritis. Furthermore, we have demonstrated that depletion of CD4+CD25+ regulatory T cells, together with transient CD4+ T lymphopenia, also did not result in the development of autoimmune gastritis, indicating that peripheral expansion of the CD4+ T cell population, per se, does not result in autoimmunity in adult mice. On the other hand, depletion of CD4+CD25+ T cells in 10-day-old euthymic mice resulted in a 30% incidence of autoimmune gastritis. These data suggest that CD4+CD25+ regulatory T cells may be important in protection against autoimmunity while the immune system is being established in young animals, but subsequently other factors are required to initiate autoimmunity.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12406391&dopt=Abstract

Med Clin (Barc). 2002 Oct 19;119(13):481-4.
[Community-acquired pneumonia: serum adenosine-deaminase activity in the aetiological diagnosis]

[Article in Spanish]

Fernandez Alvarez R, Molinos Martin L, Gullon Blanco JA, Rubinos Cuadrado G, Jimenez A, Martinez Gonzalez-Rio J.

Seccion de Neumologia, Hospital Universitario de Canarias, La Laguna, Tenerife, Espana. ENELLANerra.es

BACKGROUND: Adenosine deaminase (ADA) is a cytoplasmic enzyme which activity is increased in disorders that stimulate cells involved in the immune system. In community-acquired pneumonia (CAP), increased levels of serum ADA have been associated with the presence of atypical microorganisms as the source of the former. Previous studies have shown ADA increases in non-infectious diseases. We evaluated the factors that may influence plasmatic ADA (ADAp) levels in CAP patients. PATIENTS AND METHODS: A study with cases (245 episodes of CAP) and controls (49) was designed, and the differences in ADAp activity with regard to organisms, comorbidity factors and complications were analyzed. A logistic regression analysis was performed. RESULTS: CAP caused by atypical microorganisms were found to have increased ADAp values. Variables that independently increased ADAp levels were: atypical etiology (OR = 5.9), liver disease (OR = 5.8), diabetes mellitus (OR = 1.9), and prior antibiotic consumption (OR = 1.7). CONCLUSIONS: ADAp is an etiologic marker that could be useful in the empiric approach of the treatment of CAP.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12406394&dopt=Abstract

Pain. 2002 Oct;99(3):385-96.
Patient-related barriers to pain management: the Barriers Questionnaire II (BQ-II).

Gunnarsdottir S, Donovan HS, Serlin RC, Voge C, Ward S.

School of Nursing, University of Wisconsin-Madison, K6/333, 600 Highland Avenue, Madison, WI 53792-2455, USA. sgunnarsdottudents.wisc.edu

Patients' beliefs can act as barriers to optimal management of cancer pain. The Barriers Questionnaire (BQ) is a tool used to evaluate such barriers. Here, the BQ has been revised to reflect changes in pain management practices, resulting in the Barriers Questionnaire-II (BQ-II), a 27-item, self report instrument. This paper presents the results from two studies where the psychometric properties of the BQ-II were evaluated. In the first study, the responses of 27 nurses trained in pain management were compared to responses of a convenience sample of 12 patients with cancer. The results indicated that patients with cancer had higher mean scores on the BQ-II than did nurses trained in pain management. In the second study, a convenience sample of 172 patients with cancer responded to the BQ-II and a set of pain and quality of life (QOL) measures. A factor analysis supported four factors. Factor one, physiological effects, consists of 12 items addressing the beliefs that side effects of analgesics are inevitable and unmanageable, concerns about tolerance, and concerns about not being able to monitor changes in one's body when taking strong pain medications. Factor two, Fatalism, consists of three items addressing fatalistic beliefs about cancer pain and its management. Factor three, Communication, consists of six items addressing the concern that reports of pain distract the physician from treating the underlying disease, and the belief that 'good' patients do not complain of pain. The fourth and final factor, harmful effects, consists of six items addressing fear of becoming addicted to pain medication and the belief that pain medications harm the immune system. The BQ-II total had an internal consistency of 0.89, and alpha for the subscales ranged from 0.75 to 0.85. Mean (SD) scores on the total scale was 1.52 (0.73). BQ-II scores were related to measures of pain intensity and duration, mood, and QOL. Patients who used adequate analgesics for their levels of pain had lower scores on the BQ-II than did patients who used inadequate analgesics. The BQ-II is a reliable and valid measure of patient-related barriers to cancer pain management.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12406513&dopt=Abstract

Blood. 2003 Feb 15;101(4):1645-52. Epub 2002 Oct 24.
Successful therapy of metastatic cancer using tumor vaccines in mixed allogeneic bone marrow chimeras.

Luznik L, Slansky JE, Jalla S, Borrello I, Levitsky HI, Pardoll DM, Fuchs EJ.

Divisions of Hematopoiesis/Immunology and Hematologic Malignancies, Sidney Kimmel Cancer Center at Johns Hopkins, Baltimore, MD, USA.

A frequent outcome of allogeneic stem cell transplantation (alloSCT) in the treatment of leukemia is the destruction of the host hematolymphoid compartment and, thus, the malignancy, through the combined action of high-dose chemoradiotherapy and a T-cell-mediated graft-versus-host effect. Unfortunately, alloSCT is frequently limited by toxicity, including graft-versus-host disease (GVHD), and has not been successful in the treatment of tumors derived from solid organs. Here we report a novel cooperation between host and donor T cells in the response to a tumor cell vaccine given after a nonmyeloablative allogeneic stem cell transplantation (NST) protocol that achieves stable mixed bone marrow chimerism. Treatment of animals with NST, posttransplantation donor lymphocyte infusions (DLIs), and a vaccine, comprising irradiated autologous tumor cells mixed with a granulocyte-macrophage colony-stimulating factor (GM-CSF)-producing bystander line, results in potent and specific antitumor immunity. This combined modality immunotherapy, administered after surgical removal of the primary tumor, cured metastatic mammary cancer in most animals without inducing GVHD. Cured animals contained tumor-specific T cells of both host and donor origin, but immunodeficient hosts could not be cured by NST, DLI, and vaccine administration. Thus, transfer of allogeneic donor T cells may help break functional tolerance of a host immune system to a solid tumor, thereby providing a rationale for the generation of mixed hematopoietic chimerism by NST prior to tumor cell vaccination.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12406877&dopt=Abstract

Blood. 2003 Mar 1;101(5):1734-43. Epub 2002 Oct 24.
Therapeutic factor VIII levels and negligible toxicity in mouse and dog models of hemophilia A following gene therapy with high-capacity adenoviral vectors.

Chuah MK, Schiedner G, Thorrez L, Brown B, Johnston M, Gillijns V, Hertel S, Van Rooijen N, Lillicrap D, Collen D, VandenDriessche T, Kochanek S.

Center for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute for Biotechnology, University of Leuven, Belgium.

High-capacity adenoviral (HC-Ad) vectors expressing B-domain-deleted human or canine factor VIII from different liver-specific promoters were evaluated for gene therapy of hemophilia A. Intravenous administration of these vectors into hemophilic FVIII-deficient immunodeficient SCID mice (FVIIIKO-SCID) at a dose of 5 x 10(9) infectious units (IU) resulted in efficient hepatic gene delivery and long-term expression of supraphysiologic FVIII levels (exceeding 15 000 mU/mL), correcting the bleeding diathesis. Injection of only 5 x 10(7) IU still resulted in therapeutic FVIII levels. In immunocompetent hemophilic FVIII-deficient mice (FVIIIKO), FVIII expression levels peaked at 75 000 mU/mL but declined thereafter because of neutralizing anti-FVIII antibodies and a cellular immune response. Vector administration did not result in thrombocytopenia, anemia, or elevation of the proinflammatory cytokine interleukin-6 (IL-6) and caused no or only transient elevations in serum transaminases. Following transient in vivo depletion of macrophages before gene transfer, significantly higher and stable FVIII expression levels were observed. Injection of only 5 x 10(6) HC-Ad vectors after macrophage depletion resulted in long-term therapeutic FVIII levels in the FVIIIKO and FVIIIKO-SCID mice. Intravenous injection of an HC-Ad vector into a hemophilia A dog at a dose of 4.3 x 10(9) IU/kg led to transient therapeutic canine FVIII levels that partially corrected whole-blood clotting time. Inhibitory antibodies to canine FVIII could not be detected, and there were no signs of hepatotoxicity or of hematologic abnormalities. These results contribute to a better understanding of the safety and efficacy of HC-Ad vectors and suggest that the therapeutic window of HC-Ad vectors could be improved by minimizing the interaction between HC-Ad vectors and the innate immune system.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12406898&dopt=Abstract

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