SummaryUnder-agarose random migration, chemokinesis and chemotaxis of monocytes from 36 patients with Down's syndrome were compared to those of monocytes from 42 healthy, age-matched control children. Random migration of monocytes from patients with Down's syndrome was comparable to that of controls. In contrast, chemotaxis of monocytes from patients with Down's syndrome was significantly decreased (P < 0.001) when com~ared to that of controis, even though chemokinesis was significantly increased (P < 0.001). Age, sex, and physical development of patients with Down's syndrome or of control children included in this study had no apparent effect upon monocyte mobility. Abbreviations CS, control serum DS, Down's syndrome MP, mononuclear phagocytes ZAS, zymosan-activated serum Increased susceptibility to infection in patients with DS (22,28) may reflect several abnormalities in host defense mechanisms involving humoral and cellular immune responses (2, 17) and the inflammatory-phagocytic process (13,15,27). No defect can be singled out as the most important one, hence the definition of the immunodeficiency of DS as a complex sum of several immunologic faults of variable intensity that can change with age (4). Cellmediated immunity in DS is predominantly impaired at its effector site (34): depressed in vitro lymphocyte responses, anergy or weak delayed type hypersensitivity skin reactions and decrease in circulating T cells have been reported in patients with DS (16,17), although lymphocytosis with high counts of T and B cells may be found in older, institutionalized patients (34).MP and lymphocytes constitute the bulk of the inflammatory cells in delayed hypersensitivity reactions, MP playing a crucial role in phagocytosis as well (5). Accumulation of mononuclear cells at such inflammatory sites depends largely on their response to chemotactic signals. Poor mobilization of these cells may contribute to the weakness of delayed hypersensitivity and other inflammatory reactions in DS (6). We measured random migration, chemokinesis (enhancement of random migration) and chemotaxis (directional migration) of MP from patients with DS and compared them to those of healthy age-matched children. We employed the agarose-plate method (21), which is less expensive, simpler, and more reproducible than the Boyden chamber method, even though the relative sensitivity of the two assays is still somewhat controversial (14,19). Only MP of a mononuclear leukocytes population seem to contribute to the migration pattern using the agarose device (21). MATERIALS AND METHODSPatients and controls. Thirty-six home-cared patients with DS (Trisomy 21: 14 females, 22 males, 6 months to 7 years of age) were studied. None of the patients had leukemia, suffered of overt infection or took any medication within 2 wk of the study. Fortytwo healthy children (15 females, 27 males, 6 months to 7 years of age) undergoing elective orthopaedic surgery, and matched as closely as possible with the patients for similar age and sex were used as controls. Differe...
NKC is an important antiviral defense mechanism. Neonates have low NKC to HSV infected cells. Human blood MC cultured for 18 hr. with HSV infected cells produced a lymphokine which stimulated yjult MC-NKC from 53.0 + 10.5% to 79.8 + 12.896, (p < .Ol)in an 18 hr. Cr release assay against HSV infected target cells. This resulted in a calculated lymphokine-dependent cellular-cytotoxicity (LDCC) of 65.8%.No active lymphokine was produced in the presence of uninfected cells. LDCC lymphokine production was independent of MC donor HSV serology. Cells from colostrum of most (8110) women also produced an HSV stimulated lymphokine which mediated adult MC-LDCC (19.6 + 4.2%) and was greater (p < .05) than matched MC lymphokine activity (6.7 +2.6%) from these women. CC lymphokine production was also independent of donor HSV serology. Similarly, most (10113) pie-8 cells," precursors of s u r f a c e "~g~. b e a r i n g "~ c e l l s , a r e defined as c e l l s in hemopoietic tissues that lack surface imnunoglobulins (sIg-) but produce small amounts of cytoplasmic IgM components (cut). To determine whether Ig l i g h t chains and other heavy chains are also produced by pre-B c e l l s , we have used a f f i n i t y urified goat antibodies to human Ig determinants (u, 6 , y , a , K , A~ in imnunofluorescent and i~nnunochemical assays of bone marrow samples. A 1 1 sIgt B c e l l s and cIgt plasma cell s were costained with a mixture of anti-K and anti-A antibodies. None of the cIgf plasma c e l l s were double stained with anti-K and anti-A. Employing t h e techniques of immunofluorescence, radioimmunoprec i p i t a t i o n , and radioimmunodiffusion, the development of antibody responses t o RSV and BSA and t h e localization of immunoglobulin containing c e l l s i n t h e mammary glands, was studied i n groups of pregnant r a b b i t s a f t e r intravenous (IV), per o r a l (PO) o r transtracheal (IT) immunization with RSV and BSA during l a t e gestation. A predictable IgM and IgG and no IgA antibody response t o RSV was observed i n t h e serum. The secretory response t o RSV was charact e r i z e d by t h e regular appearance of IgA antibody i n the colostrum and milk a f t e r IT and PO immunization but not a f t e r IV immunization. The proportion of IgA staining c e l l s i n the mammary t i s s u e s was found t o be 50% higher i n the animals immunized by IT o r PO routes than by t h e IV route. No infectious virus o r RSV antigen was detected i n t h e breast. Most animals e l i c i t e d IgG anti-BSA response i n the serum, colostrum and milk, and a few evidenced IgA i n serum. However, IgA response t o BSA was notably absent i n colostrum and milk. These observations suggest independent contributions of bronchus associated and gut associated lymphoid t i s s u e t o t h e development of mammary immunity. More importantly, s i g n i f i c a n t differences e x i s t between soluble d ietary proteins and p a r t i c u l a t e v i r a l antigens i n t h e i r a b i l i t y t o induce breast milk antibodies.T CBLL E...
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