Regulation of Cyclophosphamide-Induced Eosinophilia in Contact Sensitivity: Functional Roles of Interleukin-5-Producing CD4+ Lymphocytes

2000 ◽  
Vol 203 (2) ◽  
pp. 124-133 ◽  
Author(s):  
Go Sasaki ◽  
Takahiro Satoh ◽  
Hiroo Yokozeki ◽  
Ichiro Katayama ◽  
Kiyoshi Nishioka
Keyword(s):  
Contact Sensitivity ◽  
Functional Roles ◽  
Interleukin 5 ◽  
Cd4 Lymphocytes ◽  
Sensitivity Functional

scholarly journals A Critical Temporal Window for Selectin-dependent CD4+ Lymphocyte Homing and Initiation of Late-Phase Inflammation in Contact Sensitivity

2004 ◽  
Vol 199 (9) ◽  
pp. 1223-1234 ◽  
Author(s):  
John M. Hwang ◽  
Jun Yamanouchi ◽  
Pere Santamaria ◽  
Paul Kubes
Keyword(s):  
Early Phase ◽  
Molecular Mechanisms ◽  
Late Phase ◽  
Leukocyte Recruitment ◽  
Late Response ◽  
Inflammatory Disorder ◽  
Contact Sensitivity ◽  
Microscopy Technique ◽  
Cd4 Lymphocyte ◽  
Cd4 Lymphocytes

Contact sensitivity (CS) is an inflammatory disorder characterized by early and late phases of leukocyte recruitment. We used a noninvasive intravital microscopy technique allowing for the direct visualization of leukocyte rolling and adhesion on blood vessel endothelium. By blocking specific adhesion molecules, we elucidated the molecular mechanisms mediating early leukocyte recruitment to be E- and P-selectin and demonstrated that leukocyte recruitment in the late phase had a different adhesive profile (mainly α4-integrin). Complete blockade of E- and P-selectin within the first 2 h of leukocyte–endothelial cell interactions (but not later) eliminated selectin-independent leukocyte recruitment at 24 h. Despite the predominance of neutrophils in the early phase, specific elimination of CD4+ lymphocytes in the early phase eliminated the late response. CD4+ lymphocytes homed to skin via E- and P-selectin within the early phase and induced the late phase response. Addition of these same CD4+ lymphocytes 2 h after antigen challenge was too late for these cells to home to the skin and induce late phase responses. Our data clearly demonstrate that the antigen-challenged microenvironment is only accessible to CD4+ lymphocytes for the first 2 h, and that this process is essential for the subsequent recruitment of other leukocyte populations in late phase responses.

Interleukin 5 Plays an Essential Role in Elicitation of Contact Sensitivity through Dual Effects on Eosinophils and B-1 Cells

2006 ◽  
Vol 140 (1) ◽  
pp. 8-16 ◽  
Author(s):  
Atsuko Itakura ◽  
Yuji Kikuchi ◽  
Taku Kouro ◽  
Masashi Ikutani ◽  
Satoshi Takaki ◽  
...  
Keyword(s):  
Essential Role ◽  
Contact Sensitivity ◽  
Interleukin 5

Interleukin-4, interferon-gamma and interleukin-5 in peripheral blood of children with moderate atopic asthma

1997 ◽  
Vol 27 (11) ◽  
pp. 1254-1260 ◽  
Author(s):  
M. O. HOEKSTRA ◽  
Y. HOEKSTRA ◽  
D. DE REUS ◽  
B. RUTGERS ◽  
J. GERRITSEN ◽  
...  
Keyword(s):  
Interferon Gamma ◽  
Peripheral Blood ◽  
Atopic Asthma ◽  
Interleukin 4 ◽  
Interleukin 5

Anticardiolipin Antibodies Are Elevated in HIV-1 Infected Haemophiliacs but Do Not Predict for Disease Progression

1989 ◽  
Vol 61 (01) ◽  
pp. 081-085 ◽  
Author(s):  
Simon Panzer ◽  
Christoph Stain ◽  
Hubert Hartl ◽  
Robert Dudczak ◽  
Klaus Lechner
Keyword(s):  
Normal Values ◽  
Anticardiolipin Antibodies ◽  
Haemophilia A ◽  
Serum Samples ◽  
Factor Viii Concentrates ◽  
Patient Groups ◽  
Anti Hiv ◽  
Hiv 1 ◽  
Cd4 Lymphocytes

SummaryLevels of anticardiolipin antibodies (ACA) were measured in 55 patients with haemophilia A in serum samples obtained in 1983 and in 1987. Twenty-one patients were negative for anti HIV-1 antibodies in 1983 and remained negative in 1987; 34 patients had anti HIV-1 antibodies in 1983; 17 of these latter patients remained asymptomatic, whereas 17 patients developed ARC or AIDS during the 4 years follow-up. Thirteen anti HIV-1 negative patients had elevated ACA levels in 1983; subsequently, a significant decrease was observed in all these subjects (p <0.001). All anti HIV-1 positive patients had elevated ACA levels in 1983; normal values were found in 9 patients in 1987. Yet, these changes were not significant (p >0.05). ACA levels were significantly higher in HIV-1 infected patients than in those without anti HIV-1 antibodies (p <0.05). There was no difference of ACA levels between the two anti HIV-1 positive patient groups, be it in 1983 or be it in 1987 (p >0.05). There was no correlation of ACA levels with serum IgG concentrations, CD4+ lymphocytes, or the consumption of factor VIII concentrates.

Heparin Cofactor II Deficiency in Patients Infected with the Human Immunodeficiency Virus

1993 ◽  
Vol 70 (05) ◽  
pp. 730-735 ◽  
Author(s):  
P Toulon ◽  
M Lamine ◽  
I Ledjev ◽  
T Guez ◽  
M E Holleman ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Absolute Number ◽  
Thrombin Inhibitor ◽  
Unusual Complication ◽  
Healthy Individuals ◽  
Heparin Cofactor Ii ◽  
Immunodeficiency Virus ◽  
Coagulation Inhibitor ◽  
The Mean ◽  
Cd4 Lymphocytes

SummaryIn human plasma, heparin cofactor II (HCII) is a thrombin inhibitor, whose deficiency has been reported to be associated with recurrent thrombosis. The finding of two cases of low plasma HCII activity in two patients infected with the human immunodeficiency virus (HIV) led us to investigate this coagulation inhibitor in the plasma of a larger population of HIV-infected patients. The mean plasma HCII activity was significantly lower in 96 HIV-infected patients than in 96 age- and sex-matched healthy individuals (0.75 ± 0.24 vs 0.99 ± 0.17 U/ml, p <0.0001). HCII antigen concentration was decreased to the same extent as the activity. The proportion of subjects with HCII deficiency was significantly higher in the HIV-infected group than in healthy individuals (38.5% vs 2.1%). In addition, HCII was significantly lower in AIDS patients than in other HIV-infected patients, classified according to the Centers for Disease Control (CDC) on the basis of an absolute number of circulating CD4+ lymphocytes below 200 x 106/1. The link between HCII and immunodeficiency is further suggested by significant correlations between HCII activity and both the absolute number of CD4+ lymphocytes and the CD4+ to CD8+ lymphocyte ratio. Nevertheless, the mean HCII level was not different in the various groups of patients classified according to clinical criteria, except in CDC IVD patients in whom HCII levels were significantly lower. In addition, no correlation could be demonstrated between HCII and protein S activities, another coagulation inhibitor whose plasma level was also found to be decreased in HIV-infected patients. A similar prevalence of HCII deficiency was also found in a small series of 7 HIV-infected patients who developed thrombotic episodes, an unusual complication of the infection. This suggests that, in HIV-infected patients, HCII deficiency is not in itself the causative factor for the development of thrombosis.

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