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1  driven by aberrant T-cell responses against cryptococci.
2 n to harbor highly encapsulated, replicating cryptococci.
3 -temperature adaptation and pathogenicity of cryptococci.
4 Ab to facilitate attachment and ingestion of cryptococci.
5 anner that is characteristic of encapsulated cryptococci.
6 elial cells that facilitate the migration of cryptococci across the BBB and ultimately induce endothe
7                    Birds can be colonised by cryptococci and can transmit cryptococcosis to humans vi
8 hages had increased numbers of intracellular cryptococci and YM1 crystals, indicative of alternativel
9                            A small subset of cryptococci are able to adapt to the inhibitory intracel
10 y early interactions between macrophages and cryptococci are critical in the outcome of cryptococcosi
11                                              Cryptococci are intrinsically resistant to the latest ge
12 ine model of cryptococcal meningitis whereby cryptococci are introduced directly into the CNS.
13                                The resulting cryptococci are slow-growing and acapsular.
14 H inhibits antibody-mediated phagocytosis of cryptococci by macrophages and microglia, likely due to
15 edly increases phagocytosis of non-opsonised cryptococci by murine and human macrophages.
16 yptococcal culture filtrate Ag + heat-killed cryptococci-CFA), or controls, stimulated significant in
17  to the nonprotective immunogen (heat-killed cryptococci-CFA), the nonprotective immunogen mixed with
18 fter suddenly stopping in brain capillaries, cryptococci cross into the central nervous system in a p
19                           Here, we show that cryptococci develop resistance to 5-FC at a high frequen
20 ature and a "Trojan horse" mechanism whereby cryptococci enter the central nervous system after macro
21 week-old immunized and infected mice cleared cryptococci from brain, spleen, and liver in a manner si
22  levels were elevated in cultures containing cryptococci grown in RPMI 1640 at 37 degrees C in an atm
23 rophages are central to the host response to cryptococci; however, it is unclear how C. neoformans is
24 MAbs facilitate phagocytosis of encapsulated cryptococci, (ii) some anti-GXM antibodies are opsonic i
25 Abs, stimulated phagocytosis of encapsulated cryptococci in the absence of serum.
26 vival and in decreasing the tissue burden of cryptococci in the hemocoel.
27 n earlier accumulation of C3 on encapsulated cryptococci in the presence of the Fab fragments.
28                   DC lysosomal extracts kill cryptococci in vitro; however, the means of antifungal a
29 and subpleural granulomas that harbor viable cryptococci inside macrophages and epithelioid cells.
30 ning for glucuronoxylomannan showed isolated cryptococci inside the eosinophilic cuffs.
31              However, the older mice cleared cryptococci much more efficiently from the lungs.
32                                      Inhaled cryptococci must survive the host immune response, escap
33  response to infection with either wild-type cryptococci or the mutant strain with reduced surface xy
34 crophages are able to suppress the growth of cryptococci seen in mammalian cells despite C. neoforman
35 5% decrease in phagocytosis of non-opsonised cryptococci, strongly suggesting that it is a key non-op
36 lthy individuals can maintain low numbers of cryptococci that can become a nidus for re-activation di
37 elial cells associate with, and internalize, cryptococci, they upregulate the expression of several p
38                            Following uptake, cryptococci translocate to the DC lysosomal compartment
39 ic oxide production during interactions with cryptococci was associated with decreased levels of tumo
40                                              Cryptococci were associated with eosinophils within eosi
41 onment associated with impaired clearance of cryptococci while high IL-7 levels may reflect IL-7/IL-7
42  that macrophages preferentially phagocytose cryptococci with smaller polysaccharide capsules and tha
43 macrophages: higher numbers of intracellular cryptococci, YM1 crystals, and induction of CCL17.