Biomedical subjects

M Caligiuri

Publications and source records attributed to M Caligiuri.

22 records · Page 2Linked to original sources

PubMed1989

CD3-negative natural killer cells express zeta TCR as part of a novel molecular complex.

Natural killer (NK) cells are large granular lymphocytes capable of killing tumour cells in a non-MHC restricted manner. NK cells do not express cell-surface CD3, or any known target recognition structure analogous to the T cell antigen receptor (TCR) heterodimers (alpha beta or gamma delta). Consistent with their lack of expression of a CD3-TCR complex, NK cells do not require prior sensitization or antigen presentation by accessory cells to specifically recognize their tumour targets. Although NK cells do not express CD3-TCR, they do express CD2, the target of an alternative activation pathway which is functional in both T cells and NK cells. In T cells, this alternative activation pathway utilizes some component of the CD3-TCR complex as a transducer molecule that is required for mitogenesis. The fact that NK cells are activated by this alternative pathway suggested that they might express a related subunit of the CD3-TCR complex capable of transducing the CD2-mediated signal. Here we show that human NK cells express the zeta-chain of the TCR complex in association with additional structures not included in CD3-TCR.

Antibodies, Monoclonal↗

PubMed1988

Hypoglossal, trigeminal, and facial motoneuron involvement in amyotrophic lateral sclerosis.

Facial, trigeminal, and hypoglossal motoneuron involvement was quantified in 25 amyotrophic lateral sclerosis patients and in normal controls. Measures included (1) maximum voluntary contraction of the lower lip, mandible, and tongue using custom-designed force transducers, (2) clinical functions of each muscle group, and in some patients (3) orofacial mobility using videofluoroscopy. All measures indicated that the tongue muscles were most severely affected, even in patients who initially had symptoms in the extremities.

Adult↗

PubMed1987

Phenotypic and functional deficiency of natural killer cells in patients with chronic fatigue syndrome.

Natural killer (NK)3 cells are large granular lymphocytes that appear to play a significant role in the host's defense against viral infection. We performed an extensive phenotypic and functional characterization of NK cells on 41 patients with the chronic fatigue syndrome (CFS), or "chronic active Epstein-Barr virus infection" syndrome, and on 23 age- and sex-matched asymptomatic control subjects in an attempt to further characterize this illness. These studies demonstrated that a majority of patients with CFS have low numbers of NKH1+T3- lymphocytes, a population that represents the great majority of NK cells in normal individuals. CFS patients had normal numbers of NKH1+T3+ lymphocytes, a population that represents a relatively small fraction of NK cells in normal individuals. When tested for cytotoxicity against a variety of different target cells, patients with CFS consistently demonstrated low levels of killing. After activation of cytolytic activity with recombinant interleukin 2, patients were able to display increased killing against K562 but most patients remained unable to lyse Epstein-Barr virus-infected B cell targets. Additional cytotoxicity experiments were carried out utilizing anti-T3 monoclonal antibody to block killing by NKH1+T3+ cells. These experiments indicated that the NK cell that appears to be responsible for much of the functional activity remaining in patients with CFS belongs to the NKH1+T3+ subset, which under normal circumstances represents only approximately 20% of the NK cell population.

Antibodies, Viral↗

PubMed1982

Hormonal changes and enforced diving in the harbor seal Phoca vitulina. II. Plasma catecholamines.

Plasma epinephrine and norepinephrine concentrations were measured in five harbor seals, Phoca vitulina, during a control period, during a 6-min dive, and during a 30-min postdiving recovery period. Measurements were performed with and without prior glucose administration. Control epinephrine concentrations [189 +/- 118 (SD) pg/ml] and norepinephrine concentrations (340 +/- 191 pg/ml) were similar to resting values in humans. During diving there are dramatic increases in both epinephrine and norepinephrine concentrations, which returned to control values by 30 min of the postdiving recovery period. A similar pattern was found after glucose infusion. The increased catecholamines were not the primary mechanism responsible for arterial constriction during the dive. Persistent diving bradycardia suggests obliteration of the chronotropic effects of catecholamines during the dive. An unchanged stroke volume suggests obliteration of the inotropic effects of catecholamines during the dive. Catecholamines do not appear to be involved in postdiving hyperglycemia and hyperglucogenemia. Neither the regulatory role of increased catecholamines nor the physiological function of increased catecholamines was apparent from the studies. However, dramatic increases in plasma catecholamines during diving appear to be an important component of the hormonal response to prolonged diving in aquatic mammals.

Animals↗