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1 ells, which can result in potentially lethal toxic shock.
2 ice and were also protected from SEB-induced toxic shock.
3 as a leading cause of food-borne disease and toxic shock.
4 including sepsis, necrotizing fasciitis and toxic shock.
5 be key effector cells in the pathogenesis of toxic shock.
6 sociated with severe systemic infections and toxic shock.
7 -induced lymphocyte proliferation and lethal toxic shock.
8 t attempt to associate toxin production with toxic shock.
9 ock and multiorgan failure characteristic of toxic shock.
10 ring on the pathophysiology of streptococcal toxic shock.
11 e for IL-18/IL-18Ralpha in Ehrlichia-induced toxic shock.
12 ering a potential approach in the therapy of toxic shock.
13 ller (NK) and NKT cells in Ehrlichia-induced toxic shock.
14 yndecan-1-null mice undergoing Gram-positive toxic shock.
15 ting inflammatory responses in Gram-positive toxic shock, a systemic disease that is a significant ca
16 oning, is also a superantigen that can cause toxic shock after traumatic or surgical staphylococcal w
17 MyD88(-/-) mice were resistant to SEA or SEB toxic shock and displayed reduced levels of pro-inflamma
21 an diseases including pharyngitis, impetigo, toxic shock, and necrotizing fasciitis, as well as the p
23 ar to WT mice, they did not develop signs of toxic shock, as shown by elevated bacterial burdens, low
24 sm that protects the host from Gram-positive toxic shock by inhibiting the dysregulation and amplific
25 in, rescued syndecan-1-null mice from lethal toxic shock by suppressing the production of TNFalpha an
26 ing in myriad disorders, such as dermatitis, toxic shock, cardiovascular disease, acute pelvic and ar
27 hich is known to mediate immunopathology and toxic shock in a murine model of fatal ehrlichiosis.
28 ctivation and cytokine production as well as toxic shock induced by staphylococcal enterotoxin B (SEB
30 infection with IOE resulted in acute, severe toxic shock-like syndrome and severe multifocal hepatic
31 of CD1d-restricted NKT cells in induction of toxic shock-like syndrome caused by gram-negative, lipop
32 otropic Ehrlichia strains results in a fatal toxic shock-like syndrome characterized by a decreased n
33 virulent Ehrlichia strain (IOE) results in a toxic shock-like syndrome characterized by severe liver
34 uis arthroplasty infection and streptococcal toxic shock-like syndrome due to an nonencapsulated sero
35 [IOE]) results in CD8+ T-cell-mediated fatal toxic shock-like syndrome marked by apoptosis of CD4+ T
36 ls mediate Ehrlichia-induced T-cell-mediated toxic shock-like syndrome, most likely via cognate and n
37 HME disease can range from mild to a fatal, toxic shock-like syndrome, yet the mechanisms regulating
42 oup A Streptococcus, is sufficient to induce toxic-shock-like vascular leakage and tissue injury.
45 for their therapeutic efficacy in the mouse toxic shock model using different challenge doses of SEB
47 was 11% but was much higher in patients with toxic shock syndrome (55%) and necrotizing fasciitis (58
52 e from severe cases, including streptococcal toxic shock syndrome (STSS) and necrotizing fasciitis (N
53 S) isolates from patients with streptococcal toxic shock syndrome (STSS) and necrotizing fasciitis (N
55 n A) is highly associated with streptococcal toxic shock syndrome (STSS) and other invasive streptoco
56 s associated with outbreaks of streptococcal toxic shock syndrome (STSS) in the United States and Eur
58 nd is strongly associated with streptococcal toxic shock syndrome (STSS), a severe and often fatal il
59 sult in the recently described streptococcal toxic shock syndrome (STSS), which is characterized by r
64 erantigens (PTSAgs) that are associated with toxic shock syndrome (TSS) and staphylococcal food poiso
72 uced by concentrations of the staphylococcal toxic shock syndrome (TSS) toxin 1 (TSST-1) and the stre
75 G) is sometimes administered for presumptive toxic shock syndrome (TSS), but its frequency of use and
76 icated in several serious diseases including toxic shock syndrome (TSS), Kawasaki disease, and sepsis
85 obic, Gram-positive bacterium that can cause toxic shock syndrome after gynecological procedures.
86 nkeys manifested a T cell activation-related toxic shock syndrome and a profound depletion of CD4+ ly
87 xin B (SEB) is a potent toxin that can cause toxic shock syndrome and act as a lethal and incapacitat
94 aureus group-III strains are responsible for toxic shock syndrome and have been underestimated in oth
95 auses a variety of human diseases, including toxic shock syndrome and necrotizing fasciitis, which ar
98 irulence factors and are responsible for the toxic shock syndrome and other superantigen-related dise
100 describe four deaths due to endometritis and toxic shock syndrome associated with C. sordellii that o
102 e GAS infections, including 11 streptococcal toxic shock syndrome cases and one necrotizing fasciitis
108 partial thromboplastin time in streptococcal toxic shock syndrome is associated with activation of th
109 sis of necrotizing soft-tissue infection and toxic shock syndrome resulting from Streptococcus pyogen
111 s described that specifically promote either toxic shock syndrome toxin (TSST) 1 or staphylococcal en
112 on of staphylococcal enterotoxin A (SEA) and toxic shock syndrome toxin (TSST) in neat milk without s
113 us, staphylococcal enterotoxins (SE) A-E and toxic shock syndrome toxin (TSST)-1, which are associate
115 nicity island SaPI1 carries the gene for the toxic shock syndrome toxin (TSST-1) and can be mobilized
116 IPs to S. aureus inhibited the production of toxic shock syndrome toxin (TSST-1) and enterotoxin C3,
117 dose-dependent transcytosis in vitro, while toxic shock syndrome toxin (TSST-1) exhibited increased
118 .g., carriage of the enterotoxin A (sea) and toxic shock syndrome toxin (tst) genes and production of
119 of oxygen is necessary for the production of toxic shock syndrome toxin 1 (TSST-1) by Staphylococcus
121 he effect of O(2) and CO(2) on expression of toxic shock syndrome toxin 1 (TSST-1) by Staphylococcus
124 s with staphylococcal enterotoxin B (SEB) or toxic shock syndrome toxin 1 (TSST-1) resulted in enhanc
126 T2-I-A(b), is very inefficient at presenting toxic shock syndrome toxin 1 (TSST-1) to T cells, sugges
127 ne monoclonal antibodies (MAbs) specific for toxic shock syndrome toxin 1 (TSST-1), a bacterial super
128 there have been reports of the production of toxic shock syndrome toxin 1 (TSST-1), enterotoxin, and
130 tes production of agr RNAIII, protein A, and toxic shock syndrome toxin 1 (TSST-1), particularly unde
131 r, unlike the classical enterotoxins SEB and toxic shock syndrome toxin 1 (TSST-1), the gene for SEl-
132 ught to be associated with colonization with toxic shock syndrome toxin 1 (TSST-1)-producing Staphylo
135 g., staphylococcal enterotoxin A [SEA], SEB, toxic shock syndrome toxin 1 [TSST-1]) which act both as
136 ococcal enterotoxin A (SEA), SEB, or SEC3 or toxic shock syndrome toxin 1 and a potentiating dose of
137 study the activity of superantigens such as toxic shock syndrome toxin 1 and also found that despite
138 ant Staphylococcus aureus and genes encoding toxic shock syndrome toxin 1 and Panton-Valentine leukoc
139 ttenuated staphylococcal enterotoxin (SE) or toxic shock syndrome toxin 1 develop protective antibodi
141 taphylococcal clone or structural variant of toxic shock syndrome toxin 1 is associated with Kawasaki
142 replication, and suboptimal stimulation with toxic shock syndrome toxin 1 leads to viral replication
143 staphylococcal enterotoxin B and C negative, toxic shock syndrome toxin 1 positive, and staphylococca
144 nced portions of the regions encoding mature toxic shock syndrome toxin 1 were identical in all six s
145 f staphylococcal enterotoxin A (SEA) to SEH, toxic shock syndrome toxin 1, and Panton-Valentine leuko
146 roliferation in response to the superantigen toxic shock syndrome toxin 1, as well as the proliferati
147 erum) against combinations of superantigens (toxic shock syndrome toxin 1, enterotoxins B and C, and
149 ere capable of attenuating the production of toxic shock syndrome toxin-1 (also under the control of
151 as well as the staphylococcal superantigens toxic shock syndrome toxin-1 (TSST-1) and staphylococcus
152 fine the interface between the bacterial SAG toxic shock syndrome toxin-1 (TSST-1) and the TCR, we pe
153 ee-dimensional structures of five mutants of toxic shock syndrome toxin-1 (TSST-1) have been determin
155 superantigens [staphylococcal enterotoxins, toxic shock syndrome toxin-1 (TSST-1), and streptococcal
156 Staphylococcal superantigens (SAgs), such as toxic shock syndrome toxin-1 (TSST-1), are the main caus
157 nical cases of TSS arise due to an exotoxin, toxic shock syndrome toxin-1 (TSST-1), elaborated by tox
159 ram quantities of topically applied purified toxic shock syndrome toxin-1 (TSST-1), staphylococcal en
163 We investigated whether the superantigen toxic shock syndrome toxin-1 (TSST1) could induce an ant
166 nine mutations were constructed in S. aureus toxic shock syndrome toxin-1 amino acids D120 to D130.
168 lysin streptolysin O enhanced penetration of toxic shock syndrome toxin-1 and streptococcal pyrogenic
170 d theories of Kawasaki disease etiology, the toxic shock syndrome toxin-1 hypothesis and the coronavi
173 r, a detailed structural analysis shows that toxic shock syndrome toxin-1 lacks several structural fe
176 ly express BP107 conformational epitopes and toxic shock syndrome toxin-1 superantigen-binding capabi
177 ells were stimulated with the staphylococcal toxic shock syndrome toxin-1, enterotoxin A, or enteroto
178 - and beta-toxins, but not enterotoxin A and toxic shock syndrome toxin-1, rapidly potentiated sheddi
180 enough to allow for enhanced penetration of toxic shock syndrome toxin-1, whereas streptolysin O dir
181 trains of S. aureus produce the superantigen toxic shock syndrome toxin-1, which can penetrate the va
186 es (both MSSA and MRSA) carried the gene for toxic shock syndrome toxin; however, carriage of the gen
189 esis, a strain recovered from a patient with toxic shock syndrome was serially passaged for 6 weeks,
190 ained from seven patients with streptococcal toxic shock syndrome who received IVIG therapy, and the
191 g high-risk or protection from streptococcal toxic shock syndrome with a strong protection conferred
192 bacteremia, septic arthritis, streptococcal toxic shock syndrome, and necrotizing fasciitis) caused
193 TNF release during acute TSST1-precipitated toxic shock syndrome, and the C-terminal domain to stimu
194 rious diseases, including food poisoning and toxic shock syndrome, are termed superantigens (SAgs).
195 ted in a number of human diseases, including toxic shock syndrome, diabetes mellitus and multiple scl
197 known virulence factors in scarlet fever and toxic shock syndrome, mechanisms by how SAgs contribute
198 itis, impetigo, scarlet fever, streptococcal toxic shock syndrome, necrotizing fasciitis and myositis
199 ases of severe iGAS infection (streptococcal toxic shock syndrome, necrotizing fasciitis, septic shoc
200 igens (PTSAgs) that can cause illness, e.g., toxic shock syndrome, or synergize with a number of othe
203 on of bacterial superantigens, most commonly toxic shock syndrome-1 (TSST-1), to specific TCR Vbeta-b
239 disease in epidemics and its resemblance to toxic-shock syndrome make an infectious etiology seem mo
240 anton-Valentine leukocidin, alpha-toxin, and toxic-shock syndrome toxin 1 and increased toxin product
241 Immunoblot analysis of the enterotoxins, toxic-shock syndrome toxin 1, and SpeA with antiserum pr
242 n-Valentine leukocidin, alpha-hemolysin, and toxic-shock syndrome toxin 1, in both methicillin-sensit
243 lococcus aureus enterotoxins (S.E.) A-I, and toxic-shock syndrome toxin TSST-1 act as superantigens t
248 k, we reported that the staphylococcal toxin toxic shock toxin-1 (TSST-1), a prototypic superantigen,
249 Surprisingly, 6 of 16 strains were the same toxic shock toxin-1 (TSST-1)-positive clone, designated
250 ich CD8(+) T cells mediate Ehrlichia-induced toxic shock, which is associated with IL-10 overproducti
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