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1

CD45 in memory and disease

100%
Tchilian E. Z., Beverley P. C. L.
Archivum Immunologiae et Therapiae Experimentalis
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2002
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vol. 50
|
issue 2
85-94
EN
CD45 (the leukocyte common antigen) is known to function as a tyrosine phosphatase in leucocyte signalling. Biochemical studies indicate that CD45 is involved in the regulation both of T cell receptor-associated kinases and Janus kinases that transmit signals from cytokine receptors. However the function of the different isoforms of CD45 generated by complex alternative splicing, and indeed the role of the whole extracellular domain of the molecule, remain mysterious. Analysis of CD45 knockouts and of transgenic mice expressing single CD45 isoforms, as well as the disease associations of human polymorphisms, is providing new insights into CD45 function. Accumulating data from these genetic and biochemical studies promises to elucidate the role of high and low molecular weight isoforms of CD45 in the function of na?ve and memory T lymphocytes.
2

Considerations on clinical use of T Cell immunotherapy for cancer

100%
Plautz G. E., Cohen P. A., Shu S.
Archivum Immunologiae et Therapiae Experimentalis
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2003
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vol. 51
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issue 4
245-257
EN
The recognition by effector T lymphocytes of novel antigenic targets on tumor cells is the premise of specific targeted immunotherapy of cancer. With the molecular characterization of peptide epitopes from melanoma antigens, and more recently broadly expressed tumor antigens, there has been considerable enthusiasm for clinical evaluation of peptide tumor vaccines. Immunologic monitoring of vaccinated patients has demonstrated expansion of CD8+ T cells that react with the relevant peptide and, more importantly, with native tumor. In most instances however, vaccine-induced CD8+ T cell responses alone have not been sufficiently robust or sustained to translate into a high percentage of durable clinical responses. Vaccine strategies have also utilized dendritic cells (DCs) that have been modified to present tumor antigens. The superior antigen processing capacity and co-stimulatory function of DC convey a powerful stimulatory signal to both CD4+ and CD8+ T cells. Several strategies are attempting to broaden the immune response beyond single antigens by introducing the entire complement of tumor antigens into DCs. Adoptive immunotherapy is a promising strategy to recover tumor-reactive precursor T cells from patients, stimulate them to induce numerical expansion, and then re-infuse them. Ex vivo manipulation of the tumor-reactive T cells also permits cytotoxic therapy to be administered to the patient without damaging the effector cells. Recently, host lymphodepletion prior to adoptive transfer of effector T cells has resulted in an extremely high and sustained frequency of effectors that has achieved therapeutic efficacy against bulky metastatic disease in a substantial fraction of treated patients.
3

Allergen-specific T lymphocytes as targets for specific immunotherapy: striking at the roots of type I allergy

100%
Bohle B.
Archivum Immunologiae et Therapiae Experimentalis
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2002
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vol. 50
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issue 4
233-242
EN
In the past decades allergic diseases have tremendously increased and hypersensitivity reactions now represent a growing health concern in industrialized countries. Despite various effective therapeutic options for the treatment of allergic diseases, only specific immunotherapy (SIT) has been shown to have effects on the underlying immunological mechanisms, namely functional changes at the level of T helper lymphocytes (Th). It was found that allergen-specific CD4+ Th2 lymphocytes play a key role in the pathophysiology of atopic diseases. During successful SIT, the Th2-dominated immune response is modified towards a Th1 response, leading to a decline in allergen-specific IgE levels in the long term. In order to improve the efficacy and safety of SIT, novel approaches were developed targeting allergen-specific Th2 lymphocytes since specific inactivation or modulation towards Th1 cells could interfere with the disease process. In view of this aspect, this review will basically focus on two new promising approaches to improve SIT: 1) the use of hypoallergenic proteins characterized by reduced IgE-binding capacities but retained T lymphocyte-activating properties and 2) oligodeoxynucleotides containing CpG motifs as an example of adjuvants which foster Th1 immune responses. Both approaches promise to be capable of adjusting the pathological Th2 immune response.
4

Mechanisms of mouse T lymphocyte-induced suppression of the IgG2ab allotype and T lymphocyte tolerance to IgG2ab

88%
Majlessi L., Bordenave G.
Archivum Immunologiae et Therapiae Experimentalis
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2001
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vol. 49
|
issue 6
407-416
EN
In mice of the Igha immunoglobulin allotypic haplotype we found, the presence of T lymphocytes with an inherent inhibitory activity against the expression of the IgG2ab allotype (IgG2a of the Ighb immunoglobulin allotypic haplotype). This constitutive anti-IgG2ab T lymphocyte activity can be enhanced in vivo by what we called 'sensitization', which usually consists of one or two intravenous injections of B splenocytes from Ighb congenic mice. When injected at birth, the resulting anti-IgG2ab T splenocytes induce, with 100% success, total, specific and chronic (but experimentally reversible) suppression of IgG2ab in Igha/b F1 hybrid mice prepared by mating Igh congenic mice. Even if restricted to IgG2ab expression, this experimental model, which deals with an unambiguous case of T cell-mediated down-regulation of immunoglobulin production, provides a clear and powerful tool to dissect finely the behavior of the partners (T and B lymphocytes) intervening in regulation within the immune system. For example, we observed that CD4 T lymphocytes were necessary to obtain full recruitment of anti-IgG2ab CD8 T lymphocytes during the sensitization, that suppression induction in anti-IgG2ab T splenocytes of newborn recipients required cooperation between CD4 and CD8 T lymphocytes, and that CD8 T lymphocytes were essential for suppression maintenance. We showed that this suppression was not characterized by an accumulation of B lymphocytes containing the allotype they could not secrete or Cgamma2ab mRNA they could not translate. The recipient's immune system was not involved in the suppession maintenance; this was done by donor T lymphocytes, which ensured the chronicity of IgG2ab suppression throughout the recipient's life. We demonstrated that the mechanism of this suppression implied an MHC-restricted presentation by target B lymphocytes of Cgamma2ab peptides to the T cell receptor (TCR) of anti-IgG2ab T lymphocytes. Notwithstanding the requirement of a CD4-CD8 T lymphocyte cooperation during the induction phase, we functionally determined that the suppression induction implicated an MHC class I-, but not class II-restricted interaction. We also demonstrated the existence in vivo of alternative or concomitant use of perforine- and Fas-mediated cytotoxicity pathways in this T cell-induced IgG2ab suppression. Thus this suppression did not imply silencing IgG2ab production, but B lymphocyte destruction by CD8 T lymphocytes. Always using our suppression model, we demonstrated that an agonistic anti-CD40 treatment helps in recruiting CD8 cytotoxic T lymphocytes, involved in immune regulatory functions and that CD40 expression on Ighb B lymphocytes confronted with CD8 T lymphocyte effectors only operating via the Fas pathway was involved in the total suppression of IgG2ab expression. The selection and maintenance of such normal T cell activity against the IgG2ab allotype in mice of different genetic backgrounds remain somewhat enigmatic. Indeed, we did not observe any similar activity against other immunoglobulin allotypes or isotypes. The intestinal flora had no influence on the emergence of this anti-IgG2ab T lymphocyte activity, as it was untouched in germ-free Igha mice when compared with normal Igha mice. More recently, this model offered an opportunity to study problems pertaining to immune tolerance. For instance, we showed that the genetic elements involved in the building of anti-IgG2ab TCR were available in Igha and Ighb mice of different genetic backgrounds, but that somatic constraints, namely the perinatal presence of IgG2ab, effectively prevented their acquisition, while its absence led to their spontaneous emergence. Consequently, we were able to induce anti-IgG2ab T lymphocytes into a tolerance state by injecting Igha mice with soluble IgG2ab during the perinatal period. However, the full T lymphocyte tolerance obtained in this manner was not definitively acquired, as it had reversed spontaneously when investigated 3 to 6 months after the end of tolerogen treatment, even when this treatment had been prolonged from the perinatal period to 9 months of age. The mechanisms (induction and reversion) of this tolerance involves the physical elimination or the irreversible inactivation of the natural anti-IgG2ab T lymphocyte clones and their resurgence, from bone-marrow precursors, as long as the thymus remains operational, but not the establishment of a reversible, functional unresponsiveness (anergy) or an active, cell-mediated inhibition of anti-IgG2ab T clones. We attempted to elucidate, in Ighb mice, whether the natural T lymphocyte unresponsiveness to IgG2ab involved a central tolerance mechanism and to identify the type of tolerogen implicated in this tolerogenesis. The experiments principally showed that this natural T lymphocyte tolerance to IgG2ab was mediated by a thymic mechanism; that the capacity to induce it was gradually acquired by Ighb thymuses and was most probably due to potentially IgG2ab-producing/presenting cells, progressively colonizing the developing thymus; and that a significantly decreased postnatal Cgamma2ab gene transcription correlated with the emergence of anti-IgG2ab T lymphocytes in Igha/b F1 (postnatally deprived of their B lymphocyte compartment), which subjected them to autoimmune IgG2ab-allotype suppression.
5

Cytokines in HIV-positive individuals and AIDS patients

63%
Piasecki E.
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|
vol. 49
|
issue 1
125-135
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