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PubMed2002

Immunological research in clinical psychiatry: report on the consensus debate during the 7th Expert Meeting on Psychiatry and Immunology.

There is convincing evidence that cytokines are involved in the physiology and pathophysiology of brain function and interact with different neurotransmitter and neuroendocrine pathways. The possible involvement of the immune system in the neurobiological mechanisms that underlie psychiatric disorders has attracted increasing attention in recent years. Thus in the last decade, numerous clinical studies have demonstrated dysregulated immune functions in patients with psychiatric disorders. Such findings formed the basis of the 7th Expert Meeting on Psychiatry and Immunology in Muenster, Germany, where a consensus symposium was held to consider the strengths and weaknesses of current research in psychoneuroimmunology. Following a general overview of the field, the following topics were discussed: (1) methodological problems in laboratory procedures and recruitment of clinical samples; (2) the importance of pre-clinical research and animal models in psychiatric research; (3) the problem of statistical vs biological relevance. It was concluded that, despite a fruitful proliferation of research activities throughout the last decade, the continuous elaboration of methodological standards including the implementation of hypothesis-driven research represents a task that is likely to prove crucial for the future development of immunology research in clinical psychiatry.

Allergy and Immunology↗
PubMed1988

Tools to differentiate immunologic and non-immunologic myasthenia gravis in infancy.

Twelve patients between 15 months and 13 years of age with clinical and pharmacological features of myasthenia gravis were studied. Repetitive nerve stimulation did not offer valuable information; the patients demonstrated either inspecific muscular decremental response or had normal behavior. Two clear groups of patients were identified after measurements of acetylcholine receptor (AChR) antibodies and MEPP amplitude recorded in the diaphragm of mice injected with sera from those patients. The first group included patients with positive AChR antibodies titers and decreased MEPP amplitude. The second one had negative AChR antibodies titers and MEPPs with normal amplitude. These data strongly suggest immunologic and non-immunologic mechanisms for the former and later respectively.

Action Potentials↗
PubMed1978

Multi-system immunologically mediated disease: T lymphocyte deficiency and thyroid immunologic disease--a report of four cases.

Four cases are described of multi-system immunologically-mediated disease (systemic lupus erythematosus (two cases), polymyositis, and sarcoidosis) in association with thyroid autoimmunity. In all patients there was evidence of T lymphocyte deficiency, namely poor response of peripheral blood lymphocytes (PBL) to T cell mitogens (four cases) and failure or decreased ability to become sensitized to dinitrochlorobenzene (three cases), although two patients were ill and two were being treated with steroids. There was also evidence of B lymphocyte deficiency since PBL of no patient responded normally to pokeweed mitogen, a B and T lymphocyte mitogen. In two patients there was evidence of cell-mediated immunity to human thyroid antigens. Although thyroid stimulating antibody was not detected in the one patient with Graves' disease tested, significant titres of thyroid antibodies were detected in all cases. Possible relationships between T lymphocyte deficiency, organ-specific autoimmune disease and immunologically-mediated multi-system disorders are discussed.

Adult↗
PubMed2000

[Immunology in the 20th century--progress made in research on infectious and immunological diseases].

The new era of the modern medicine was opened 100 years ago by Robert Koch and Louis Pasteur who demonstrated that various infectious diseases were caused by their respective microbes. Koch discovered Mycobacterium tuberculosis, the causative agent of tuberculosis. The first breakthrough in the modern medicine to combat against infectious diseases was the discovery of anti-diphtheria toxin antibody by E.A. von Behring and S. Kitasato. The concept of immunity--immune from disease--has thus been established. The immune response between antigen and antibody sometimes provides the host with a harmful effect. The concept of allergy was introduced by Richet and later by Prausnitz and Küstner. Why the same immune response leads to the different outcome, immunity or allergy had not been made clear until the discovery of IgE by Drs. Kimishige and Teruko Ishizaka in 1968: The IgG antibody plays a role in immunity whereas IgE antibody is involved in allergy. Tuberculin skin reaction which is well known as the diagnostic tool for mycobacterial infection was studied by M. Chase in 1945 demonstrating that it was able to be transferred to the healthy individual by immune cells but not by antibody. The immune response is now categorized into two; soluble immunity--immediate type allergy and cell-mediated immunity--delayed type allergy. The rapid progress in the molecular biology in the past decades has also accelerated the progress in immunology, several of which include discovery of two types of lymphocytes; T and B cells; concept of two T cells; Th1 and Th2 cells; and the discovery of cytokines which regulate immune cell responses. The mechanism of the immune response is now understood at the gene level. Several immunological diseases can now be successfully treated by controlling the levels of cytokines involved. For example, refractory rheumatoid arthritis is now under control by the administration of recombinant soluble TNF receptor molecules to the patients. The complete human genome sequence is currently under investigation. We can now envisage the advent of the days when every disease can be diagnosed and intervened at the gene level.

Allergy and Immunology↗
PubMed2005

Medical devices; immunology and microbiology devices; classification of AFP-L3% immunological test systems. Final rule.

The Food and Drug Administration (FDA) is classifying AFP-L3% (alpha-fetoprotein L3 subfraction) immunological test systems into class II (special controls). The special control that will apply to the device is the guidance document entitled "Class II Special Controls Guidance Document: AFP-L3% Immunological Test Systems." The agency is classifying the device into class II (special controls) in order to provide a reasonable assurance of safety and effectiveness of the device. Elsewhere in this issue of the Federal Register, FDA is announcing the availability of a guidance document that will serve as the special control for the device.

Device Approval↗
PubMed1980

[Immunologic mechanisms of specific hyposensitization in allergic diseases of an infectious nature. III. Immunologic processes in hyposensitization with microbial allergens].

The work contains the results obtained in the study of immunological processes in the dynamics of specific hyposensitization with microbial allergens, prepared from Proteus and staphylococci, in 22 infectious allergic bronchial asthma patients sensitized to these microorganisms. The therapeutic effect of this treatment was accompanied by the activation of the processes of cellular and humoral immunity, while the aggravation of the main disease was observed in patients with a pronounced decrease in the activity of immunological processes which were unaffected by the stimulating influence of specific hyposensitization.

Allergens↗
PubMed1998

A study of the immunology of the chronic fatigue syndrome: correlation of immunologic parameters to health dysfunction.

Surface and intracellular immunologic and apoptotic markers and functional lymphocyte assays after stimulation with anti-CD3/anti-CD28 antibodies or phytohemagglutinin (PHA) were studied in 44 patients fulfilling the Oxford criteria for chronic fatigue syndrome (CFS). Results were then correlated to scores for the Short Form-36 health questionnaire (SF-36), which assesses eight aspects of patient's well-being, and for the general health questionnaire (GHQ), which detects current psychiatric disorder. Patients had significantly increased mean fluorescence intensity readings of HLA-DR in CD4 and CD8 cells (P < 0.05). Expression of the costimulatory receptor CD28 in CD8 cells was significantly reduced, and the apoptosis repressor ratio of bcl-2/bax in both CD4 and CD8 was increased in patients (P < 0.05). Patients with increased HLA-DR expression had significantly lower SF-36 total scores, worse body pains, and poorer general health perception and physical functioning scores. Increased spontaneous lymphocyte proliferation was associated with poor general health perception. PHA proliferative responses were lower in patients with poor emotional and mental health scores, and the anti-CD3/anti-CD28 response was low in those with low general health perception scores. Higher spontaneous proliferation and reduced PHA responses correlated with higher GHQ scores. Similarly, GHQ scores were significantly higher, indicating worse mental health, in those with lower total SF-36 scores and worse general and mental health scores in the SF-36 questionnaire. Finally, higher expression of the costimulatory molecule CD28 correlated with higher total SF-36 scores, general health perception and social functioning scores, and with lower role limitation due to physical health. The increased expression of class II antigens and the reduced expression of the costimulatory receptor CD28, which is a marker of terminally differentiated cells, lend further support to the concept of immunoactivation of T-lymphocytes in CFS and may be consistent with the notion of a viral etiopathogenesis in the illness. We report, for the first time, increased expression of the apoptosis repressor protein bcl-2, which may contribute to enhanced survival of activated lymphocytes. Using the SF-36 health assessment questionnaire and the GHQ, we demonstrated changes in different immunological parameters, each of which correlated with particular aspects of disease symptomatology.

Adult↗
PubMed1976

Immunological and non-immunological mechanisms of some of the desirable and undesirable effects of anti-inflammatory and analgesic drugs.

Studies were carried out on patients with adverse reactions to aspirin, paracetamol, phenacetin, codeine, dihydrocodeine, some pyrazolone derivatives, and indomethacin. Three clinico-pathological forms of adverse reactions received particular attention: (1) Asthma, with or without manifestations of systemic anaphylaxis; (2) Serum-sickness-like syndrome; (3) Lymph node enlargement with histological features simulating lymphoma or Hodgkin's disease, which occurred in patients receiving phenylbutazone in particular. A variety of immunological investigations, including some in vitro correlates of immediate- or delayed-type allergy, were carried out. The three syndromes seemed to be associated with immediate-type (or immediate-type-like), immediate-type plus delayed-type, and delayed-type allergy, respectively. In most of the patients with immediate-type-like reactions, and where immunological mechanisms were apparently not involved, pharmacological mediators, particularly histamine, were released from their leucocytes when challenged in vitro with the causative agent(s). This suggested that the main underlying abnormality of their asthma or peripheral vascular manifestations was a direct release of mediators by the drugs, i.e. some type of idiosyncrasy. The causative mechanism of this abnormality has not been established yet.

Anaphylaxis↗
PubMed1984

Histamine release from the cultured mouse mast cell line PT18 in response to immunologic and non-immunologic stimuli.

Cultured mouse mast cells that are dependent on spleen-derived factors for their proliferation and maintenance have been shown rapidly to release histamine in response to immunologic stimuli, concanavalin A, and ionophores A23187 and Br-x537A. These cells did not, however, release histamine when treated with compound 48/80 or adenosine 5'-triphosphate. Immunologically mediated histamine release was inhibited by theophylline and quercetin, but not by disodium cromoglycate. The results presented here are discussed in terms of the possible relationship of this cell line to mucosal mast cells.

Adenosine Triphosphate↗
PubMed2003

The endogenous, immunologically active peptide apelin inhibits lymphocytic cholinergic activity during immunological responses.

We investigated the effects of apelin, an immunologically active peptide ligand for orphan receptor APJ, on acetylcholine (ACh) synthesis in MOLT-3 human leukemic T cells. We initially confirmed expression of APJ mRNA in several human T- and B-cell lines by reverse transcription-polymerase chain reaction (RT-PCR). We also found that in phytohemagglutinin (PHA)-stimulated MOLT-3 cells, an active apelin fragment, apelin-13, down-regulates expression of choline acetyltransferase (ChAT) mRNA and significantly reduces ChAT activity and cellular ACh content and release. It thus appears that apelin inhibits lymphocytic cholinergic activity via APJ during immunological responses.

Acetylcholine↗
PubMed2001

Can Langerhans cell UV injury and dendritic cell infection by immunodepressive viruses induce immunologic tolerance? Second part: immunologic tolerance in AIDS.

In the first part of the present editorial [1], we recalled experimental and clinical data demonstrating that 1) UV, via their effects on Langerhans cells, and 2) some so-called immunodepressive viruses, such as measles, lymphocytic choriomeningitis agents, and some animal retroviruses, via their action on dendritic cells, can induce tolerance in some conditions concerning immunologic parameters and/or the antigen(s). We present in this second part of the editorial a commentary on patients treated at the AIDS phase of HIV-1 infection for 3.5 to 8 years. Among them, one has been submitted before and at the beginning of our treatment, for a psoriasis, to a PUVA irradiation, at the dose of 214.5 J (spectrum 230-320). We were present at the end of this irradiation to see the disappearance of his blood CD4 and of his suppressor T cells. Comparing his data with those of other patients of the cohort similarly treated, we have found arguments to consider that this UV-victim patient has presented for the 6 years of his clinically excellent survival and still presents manifestations of immunologic tolerance towards a fraction of his HIV-1 population.

Acquired Immunodeficiency Syndrome↗
PubMed2000

Dissection of the enzymatic and immunologic functions of macrophage migration inhibitory factor. Full immunologic activity of N-terminally truncated mutants.

Macrophage migration inhibitory factor (MIF) is a cytokine with broad regulatory functions in innate immunity. MIF belongs to the few cytokines displaying catalytic activities, i.e. MIF has a Pro2-dependent tautomerase and a Cys-Ala-Leu-Cys (CALC) cysteine-based thiol-protein oxidoreductase activity. Previous studies have addressed the roles of the catalytic site residues and the C-terminus. The two activities have not been directly compared. Here we report on the N-terminal mutational analysis and minimization of MIF and on a dissection of the two catalytic activities by comparing mutants P2AMIF, Delta4MIF, Delta5MIF, Delta6MIF, Delta7MIF, Delta8MIF, and Delta10MIF with the cysteine mutants of MIF. As N-terminal deletion was predicted to interfere with protein structure due to disruption of the central beta sheet, it was surprising that deletion of up to six N-terminal residues resulted in normally expressed proteins with wild-type conformation. Strikingly, such mutants exhibited full MIF-specific immunologic activity. While mutation of Pro2 eliminated tautomerase activity, the CALC cysteine residues had no influence on this activity. However, mutant C81SMIF, which otherwise has full biologic activity, only had 32% tautomerase activity. Deletion of four N-terminal residues did not interfere with insulin reduction by MIF. By contrast, reduction of 2-hydroxyethyldisulfide (HED) was markedly affected by N-terminal manipulation, with P2AMIF and Delta2MIF exhibiting 40% activity, and Delta4MIF completely failing to reduce HED. This study constitutes the first comparison of the two catalytic activities of MIF and should assist in understanding the molecular links between the catalytic and immunologic activities of this cytokine and in providing guidelines for N-terminal protein minimization.

Amino Acid Sequence↗
PubMed2006

Advances in immunology: from bench to bedside--a symposium at the 2005 Annual Meeting of the Federation of Clinical Immunology Societies (FOCIS), Boston, MA, USA.

The American Uveitis Society sponsored a symposium at the recent 2005 Annual FOCIS meeting in Boston, MA, USA, that was organized by the authors of this report. The symposium was designed to bring together several leaders in the broad field of immunology and investigators in ocular immunology to discuss three interrelated areas of interest: (i) animal models of ocular inflammation; (ii) interface of innate and adaptive immunity; and (iii) immune regulation. A brief summary of the salient points of the symposium is given.

Adaptation, Physiological↗
PubMed1984

Immunologic methods in cytology: definitive diagnosis of non-Hodgkin's lymphomas using immunologic markers for T- and B-cells.

The cytologic diagnosis of malignant lymphoma can be extremely difficult because the cytologic features of the malignant cells in small cell and mixed small and large cell lymphomas may be indistinguishable from those of reactive lymphoid cells. In addition, large cell lymphoma can be difficult to distinguish from undifferentiated carcinoma in cytologic specimens. Using the avidin-biotin immunoperoxidase technic and antibodies to the B-cell markers alpha, gamma, and mu heavy chains and kappa and lambda light chains, to the T-cell markers Leu-1, Leu-2a, and Leu-3a, to the lymphoid marker T200, to TdT, and to Leu-M3, the authors studied 35 cytologic specimens including pleural, cerebrospinal, and ascites fluids and fine-needle aspirations. Immunologic staining allowed them to make a definitive diagnosis of lymphoma or reactive effusion in every case studied and resulted in a significant modification of the morphologic diagnosis in over 50% of cases. In 16 cases the lymphoid cells were monoclonal B-cells: ten expressing IgM kappa; four expressing IgM lambda; one expressing IgA kappa; and one expressing kappa without demonstrable heavy chain expression. Although there are no good markers of monoclonality for T-cells, the authors were able to make a positive diagnosis in two cases of T-cell lymphoid malignancies by the expression of an aberrant phenotype on the malignant cells. The expression of TdT confirmed the diagnosis in one case of common ALL and one lymphoblastic lymphoma. In a patient with a "null cell" large cell lymphoma, the expression of T200 on the malignant cells ruled out the possibility of carcinoma. In 15 cases the marker studies indicated a reactive lymphoid proliferation. The authors conclude that immunologic markers are very useful in the cytologic diagnosis of lymphoma.

Adolescent↗
PubMedDate not supplied

Reproductive immunology: 4. The effect of seminal plasma from immunologic infertile men on in vitro lymphocyte cultures.

The seminal plasma of 31 patients were examined for the presence of sperm antibodies and for inhibitory properties on the transformation rates of donor lymphocytes cultured in vitro. Twenty five (80%) of the men revealed apart from fertile semen, no sperm antibody activities while six (20%) patients showed high spermagglutinating antibody titres in their seminal plasma and blood serum. Following the routine semen analyses and sperm antibody estimations the seminal plasma were used in lymphocyte transformation studies in order to examine their inhibitory effect. The influence of the seminal plasmas on the lymphocytes were expressed as a percentage inhibition. The percentage inhibition of the normozoospermic men differed significantly from the immunologic infertile man (p less than 0,05). We concluded from the study that the inhibitory potential of the seminal plasma from immunologic infertile male with a normal sperm count are elevated compared with that of normozoospermic men without sperm antibodies. It also appears as if the sperm antibodies in the seminal fluid are able to bind with the inhibitory factor thus causing an enhanced inhibition effect on the lymphocytes.

Antibodies↗
PubMed1985

Evidence against HLA and immunological dependence of disease outbreak in SLE. Immunological characterisation of identical twins clinically discordant for SLE.

Identical female twins clinically discordant for 20 years for SLE were studied. Their HLA-haplotype was A1,28; B8w6,w35; Cw3,w7; Dr3,4. Both twins had a raised erythrocyte sedimentation rate, autoantibodies, and circulating immune complexes. The diseases sibling had a reversed OKT4/OKT8 ratio (0.43), decreased helper T cell number, defective pokeweed mitogen (PWM) induced plasma cell differentiation, and overactive hydrocortisone sensitive suppressor cells. Immunological abnormalities may be only partly HLA related (B8; Dr3), but are most probably secondary to the disease process in the sibling with SLE. Exogenous and/or endogenous factor(s) other than genetic or immunological are suggested as being operative in the predisposition to and expression of SLE.

Adult↗
PubMed1991

Immunological analysis of acquired factor VIII inhibitor in a case with immunologic disorder.

Coagulation factor VIII inhibitor arising in a patient with autoimmune disease was immunologically analyzed. A 63-year-old man who had been diagnosed as suffering from polyarteritis nodosa was treated with prednisolone for 10 years. Severe bleeding tendency developed and coagulation studies demonstrated a high titer of inhibitor to factor VIII:C. As a result of immunological analysis, the inhibitor was found to be IgG type autoantibody having both kappa and lambda light chains. The subclasses were IgG1 and IgG4. The inhibitor recognized the COOH-terminal light chain (72-kDa thrombin fragment) on the factor VIII molecule as an epitope.

Autoantibodies↗
PubMed1997

Immunological gene therapy approaches for malignant melanoma. 1. Tumor-immunological background.

Gene therapy approaches pursuing immunological strategies for the treatment of malignant melanoma play major roles in the current efforts to explore the potential benefits of gene transfer technologies for medicine. This may be explained by the nearly complete resistance of advanced metastatic melanoma towards conventional non-surgical treatment modalities, and the particular immunogenicity of melanoma in connection with a presumed immuno-gene therapeutic 'field effect'. The latter relates to the potency of the immune system to amplify gene transfer effects that are limited due to the imperfection of the currently available gene delivery systems. The ongoing clinical trials focus predominantly on treatment safety and tolerability rather than efficacy. The corresponding tumor-immunological background is reviewed, focusing on a treatment concept centred on tumor-reactive, cytotoxic CD8+ T effector cells.

CD8-Positive T-Lymphocytes↗