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1 e that an oral vaccination strategy prevents Pneumocystis infection.
2 l cell wall carbohydrates are induced during Pneumocystis infection.
3 with a restricted BCR were unable to control Pneumocystis infection.
4  to become fully functional in this model of Pneumocystis infection.
5 roteins for diagnostics and therapeutics for Pneumocystis infection.
6 re required for optimal host defense against Pneumocystis infection.
7 f IFN-gamma, granzyme B, and perforin during Pneumocystis infection.
8 should be taken into account when diagnosing Pneumocystis infection.
9 n CD4(+) cells was increased at 5 weeks post-Pneumocystis infection.
10 ues examined were markedly reduced following Pneumocystis infection.
11 ells play a key role in host defense against Pneumocystis infection.
12 itive cells, but did not impact clearance of Pneumocystis infection.
13 ay an important role in host defense against Pneumocystis infection.
14 endent on the ongoing resolution of a viable Pneumocystis infection.
15 dependent upon the resolution of the ongoing Pneumocystis infection.
16 y prevent bone marrow failure in response to Pneumocystis infection.
17 phages is in part due to apoptosis caused by Pneumocystis infection.
18 s can determine pulmonary complications from Pneumocystis infection.
19 ntial target for therapeutic intervention in Pneumocystis infection.
20 nd interactions are critical for controlling Pneumocystis infection.
21  mice, IL-17A is not required for control of Pneumocystis infection.
22                                We found that Pneumocystis infection accelerated osteoclastogenesis as
23  no correlation between time of diagnosis of Pneumocystis infection and change in antibody levels.
24 rated that anti-CD20 alone is permissive for Pneumocystis infection and that anti-CD20 impairs compon
25 ells from mice treated with anti-CD20 during Pneumocystis infection are incapable of mounting a prote
26                               A highly focal Pneumocystis infection associated to increased mucus exp
27 inflammation and lung injury associated with Pneumocystis infection both in the setting of immune rec
28         The immune response protects against Pneumocystis infection but is also a key component of Pn
29 hus, MyD88 is not required for resistance to Pneumocystis infection, but limits the adaptive immune r
30 the hemopoietic system under the pressure of Pneumocystis infection, but not during steady-state hemo
31 sive fungal infections (IFI) (aspergillosis, Pneumocystis infection, candidiasis, and possible IFI) a
32                                              Pneumocystis infection caused a significant increase in
33                                              Pneumocystis infection causes increased intracellular le
34           We used a cohousing mouse model of Pneumocystis infection, combined with flow cytometry and
35 s required by Pneumocystis carinii in vitro, Pneumocystis infection depletes plasma AdoMet of rats an
36                                              Pneumocystis infection generates a strong type II respon
37 n the inflammatory response directed against Pneumocystis infection has not been fully elucidated.
38 stismurina We also examined the clearance of Pneumocystis infection in IL-17A-deficient mice.
39  production in the lungs is increased during Pneumocystis infection in immunocompetent mice, IL-17A i
40                                              Pneumocystis infection in SP-A-deficient mice was associ
41 use model in which PH occurs as a sequela of Pneumocystis infection in the context of transient CD4 d
42                     The burden of nosocomial Pneumocystis infections in transplantation units in Fran
43                                              Pneumocystis infections increase host susceptibility to
44           Therefore, documenting subclinical Pneumocystis infection induces lung disease in the immun
45                             An early step in Pneumocystis infection involves the attachment of organi
46                The innate immune response to Pneumocystis infection is not well understood.
47                          Subclinical primary Pneumocystis infection is the most common pulmonary infe
48 type and IFN-alpha receptor (IFNAR) KO mice, Pneumocystis infection leads to an eosinophilic granuloc
49 lid correlative marker of lung damage during Pneumocystis infection, neither neutrophils nor ROS appe
50 e model presented here involving a localized Pneumocystis infection of the lung, followed 2 wk later
51 ient mice (IFrag-/-) to study the effects on Pneumocystis infection of the lung.
52                                              Pneumocystis infection or antigen treatment was used to
53  autopsies were excluded because of viral or pneumocystis infection or secondary bacterial infection
54 hymopoietic response in host defense against Pneumocystis infection, Pneumocystis murina infection in
55                                              Pneumocystis infection probably occurs in most humans du
56     The results of this study suggested that Pneumocystis infection results in accumulation of high l
57               In the absence of CD4 T cells, Pneumocystis infection results in vigorous CD8 T cell in
58  Taken together with the peak age of primary Pneumocystis infection, results warrant investigating th
59 A-deficient mice had developed a more severe Pneumocystis infection than CD4-depleted WT (P. carinii
60 siveness of neonatal alveolar macrophages to Pneumocystis infection that is both intrinsic and relate
61 porters of on-demand hematopoiesis following Pneumocystis infection that would otherwise be hampered
62 enitor activity during systemic responses to Pneumocystis infection, thus promoting replenishment of
63 hase were fully functional and able to clear Pneumocystis infection upon adoptive transfer into Rag1(
64                                              Pneumocystis infection was capable of priming a Th2 resp
65  The role of MyD88 in early responses during Pneumocystis infection was supported by in vivo studies
66 dying the role of type I IFNs in immunity to Pneumocystis infection, we discovered that mice lacking
67 ata1(tm6Sho)/J mice were more susceptible to Pneumocystis infection when compared with BALB/c control
68 ll as purified B cells, were able to control Pneumocystis infection, while B cell-depleted splenocyte
69 ing infection, IL-17A-deficient mice cleared Pneumocystis infection with kinetics similar to C57BL/6
70 ucan and chitosan/chitin are generated after Pneumocystis infection, with increased quantities within